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3. Epicutaneous Staphylococcus aureus induces IL-36 to enhance IgE production and ensuing allergic disease

Author

Patrick, Garrett J, Liu, Haiyun, Alphonse, Martin P, Dikeman, Dustin A, Youn, Christine, Otterson, Jack C, Wang, Yu, Ravipati, Advaitaa, Mazhar, Momina, Denny, George, Ortines, Roger V, Zhang, Emily, Miller, Robert J, Dillen, Carly A, Liu, Qi, Nolan, Sabrina J, Nguyen, Kristine, Marcello, LeeAnn, C., Danh, Wier, Eric M, Zhang, Yan, Caviness, Gary, Klimowicz, Alexander C, Mierz, Diane V, Fine, Jay S, Sun, Guangping, Goldbach-Mansky, Raphaela, Marusina, Alina I, Merleev, Alexander A, Maverakis, Emanual, Garza, Luis A, Milner, Joshua D, Gao, Peisong, Ramanujam, Meera, Raymond, Ernest L, Archer, Nathan K, and Miller, Lloyd S

Subjects
Eczema / Atopic Dermatitis, Infectious Diseases, Food Allergies, Lung, Emerging Infectious Diseases, Aetiology, 2.2 Factors relating to the physical environment, 2.1 Biological and endogenous factors, Inflammatory and immune system, Skin, Animals, Cell Differentiation, Dermatitis, Atopic, Humans, Immunoglobulin Class Switching, Immunoglobulin E, Interleukin-1, Interleukin-4, Keratinocytes, Mice, Mice, Knockout, Plasma Cells, Staphylococcus aureus, Allergy, Cytokines, Immunology, Inflammation, Medical and Health Sciences
Abstract

IgE induced by type 2 immune responses in atopic dermatitis is implicated in the progression of atopic dermatitis to other allergic diseases, including food allergies, allergic rhinitis, and asthma. However, the keratinocyte-derived signals that promote IgE and ensuing allergic diseases remain unclear. Herein, in a mouse model of atopic dermatitis-like skin inflammation induced by epicutaneous Staphylococcus aureus exposure, keratinocyte release of IL‑36α along with IL-4 triggered B cell IgE class-switching, plasma cell differentiation, and increased serum IgE levels-all of which were abrogated in IL-36R-deficient mice or anti-IL‑36R-blocking antibody-treated mice. Moreover, skin allergen sensitization during S. aureus epicutaneous exposure-induced IL-36 responses was required for the development of allergen-specific lung inflammation. In translating these findings, elevated IL‑36 cytokines in human atopic dermatitis skin and in IL‑36 receptor antagonist-deficiency patients coincided with increased serum IgE levels. Collectively, keratinocyte-initiated IL‑36 responses represent a key mechanism and potential therapeutic target against allergic diseases.

Published
2021

7. Development of a Staphylococcus aureus reporter strain with click beetle red luciferase for enhanced in vivo imaging of experimental bacteremia and mixed infections.

Author

Miller, Robert J, Crosby, Heidi A, Schilcher, Katrin, Wang, Yu, Ortines, Roger V, Mazhar, Momina, Dikeman, Dustin A, Pinsker, Bret L, Brown, Isabelle D, Joyce, Daniel P, Zhang, Jeffrey, Archer, Nathan K, Liu, Haiyun, Alphonse, Martin P, Czupryna, Julie, Anderson, William R, Bernthal, Nicholas M, Fortuno-Miranda, Lea, Bulte, Jeff WM, Francis, Kevin P, Horswill, Alexander R, and Miller, Lloyd S

Subjects
Animals, Mice, Inbred C57BL, Rabbits, Mice, Pseudomonas aeruginosa, Staphylococcus aureus, Bacteremia, Pseudomonas Infections, Staphylococcal Infections, Wound Infection, Luciferases, Diagnostic Imaging, Luminescent Measurements, Genes, Reporter, Female, Male, Coinfection, Coleoptera
Abstract

In vivo bioluminescence imaging has been used to monitor Staphylococcus aureus infections in preclinical models by employing bacterial reporter strains possessing a modified lux operon from Photorhabdus luminescens. However, the relatively short emission wavelength of lux (peak 490 nm) has limited tissue penetration. To overcome this limitation, the gene for the click beetle (Pyrophorus plagiophtalamus) red luciferase (luc) (with a longer >600 emission wavelength), was introduced singly and in combination with the lux operon into a methicillin-resistant S. aureus strain. After administration of the substrate D-luciferin, the luc bioluminescent signal was substantially greater than the lux signal in vitro. The luc signal had enhanced tissue penetration and improved anatomical co-registration with infected internal organs compared with the lux signal in a mouse model of S. aureus bacteremia with a sensitivity of approximately 3 × 104 CFU from the kidneys. Finally, in an in vivo mixed bacterial wound infection mouse model, S. aureus luc signals could be spectrally unmixed from Pseudomonas aeruginosa lux signals to noninvasively monitor the bacterial burden of both strains. Therefore, the S. aureus luc reporter may provide a technological advance for monitoring invasive organ dissemination during S. aureus bacteremia and for studying bacterial dynamics during mixed infections.

Published
2019

8. Clonal Vγ6+Vδ4+ T cells promote IL-17–mediated immunity against Staphylococcus aureus skin infection

Author

Marchitto, Mark C, Dillen, Carly A, Liu, Haiyun, Miller, Robert J, Archer, Nathan K, Ortines, Roger V, Alphonse, Martin P, Marusina, Alina I, Merleev, Alexander A, Wang, Yu, Pinsker, Bret L, Byrd, Angel S, Brown, Isabelle D, Ravipati, Advaitaa, Zhang, Emily, Cai, Shuting S, Limjunyawong, Nathachit, Dong, Xinzhong, Yeaman, Michael R, Simon, Scott I, Shen, Wei, Durum, Scott K, O’Brien, Rebecca L, Maverakis, Emanual, and Miller, Lloyd S

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Microbiology, Clinical Sciences, Immunology, Emerging Infectious Diseases, Immunization, Biodefense, Infectious Diseases, 2.1 Biological and endogenous factors, Inflammatory and immune system, Infection, Animals, Disease Models, Animal, Humans, Interleukin-17, Lymph Nodes, Mice, Staphylococcal Infections, Staphylococcus aureus, T-Lymphocyte Subsets, T-Lymphocytes, IL-17, T cells, neutrophils, skin
Abstract

T cell cytokines contribute to immunity against Staphylococcus aureus, but the predominant T cell subsets involved are unclear. In an S. aureus skin infection mouse model, we found that the IL-17 response was mediated by γδ T cells, which trafficked from lymph nodes to the infected skin to induce neutrophil recruitment, proinflammatory cytokines IL-1α, IL-1β, and TNF, and host defense peptides. RNA-seq for TRG and TRD sequences in lymph nodes and skin revealed a single clonotypic expansion of the encoded complementarity-determining region 3 amino acid sequence, which could be generated by canonical nucleotide sequences of TRGV5 or TRGV6 and TRDV4 However, only TRGV6 and TRDV4 but not TRGV5 sequences expanded. Finally, Vγ6+ T cells were a predominant γδ T cell subset that produced IL-17A as well as IL-22, TNF, and IFNγ, indicating a broad and substantial role for clonal Vγ6+Vδ4+ T cells in immunity against S. aureus skin infections.

Published
2019

9. Keratinocyte-derived defensins activate neutrophil-specific receptors Mrgpra2a/b to prevent skin dysbiosis and bacterial infection

Author

Dong, Xintong, Limjunyawong, Nathachit, Sypek, Elizabeth I., Wang, Gaofeng, Ortines, Roger V., Youn, Christine, Alphonse, Martin P., Dikeman, Dustin, Wang, Yu, Lay, Mark, Kothari, Ruchita, Vasavda, Chirag, Pundir, Priyanka, Goff, Loyal, Miller, Lloyd S., Lu, Wuyuan, Garza, Luis A., Kim, Brian S., Archer, Nathan K., and Dong, Xinzhong

Published
2022
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10. Targeted dual biologic therapy for erythroderma of unknown etiology guided by high-parameter peripheral blood immunophenotyping.

Author

Cornman, Hannah L., Alphonse, Martin P., Dykema, Arbor, Kollhoff, Alexander L., Lee, Kevin K., Manjunath, Jaya, Ma, Emily Z, Parthasarathy, Varsha, Deng, Junwen, Pritchard, Thomas, Kambala, Anusha, Marani, Melika, Parr, Kayla A., Mohammed, Javid P., Kwatra, Madan M., Bream, Jay H., Ho, Won Jin, and Kwatra, Shawn G.

Subjects
*MONONUCLEAR leukocytes, *PATHOLOGY, *PITYRIASIS rubra, *WHOLE genome sequencing, *CELL populations
Abstract

Erythroderma is a severe and heterogeneous inflammatory skin condition with little guidance on the approach to management in cases of unknown etiology. To guide therapeutic selection, we sought to create an immunophenotyping platform able to identify aberrant cell populations and cytokines in subtypes of erythroderma. We performed high-parameter flow cytometry on peripheral blood mononuclear cells (PBMCs) and whole blood of a patient with refractory idiopathic erythroderma, erythrodermic patients with Sézary syndrome and pityriasis rubra pilaris, and healthy controls. We found that the index patient had a novel form of erythroderma characterized by increased interleukin (IL)-13- and IL-17-producing γVδ2 T cells, basophils, and activated platelets. Whole-genome sequencing of PBMCs and immunofluorescence staining of skin biopsies revealed increased expression of Th2- (IL-13, IL-4Rα) and Th17-associated markers (IL-17, IL-17Rα) and non-functional mutations associated with Th2 and Th17 signaling, demonstrating that PBMCs can reflect cutaneous disease pathology. Targeted intervention via dual dupilumab and secukinumab therapy resulted in complete disease control and reduction of immunopathogenic cell populations and cytokines. This study highlights a novel form of erythroderma with concomitant Th2 and Th17 dysregulation and introduces a minimally invasive peripheral blood-based immunophenotyping platform that offers a personalized medicine approach to the management of systemic inflammatory diseases. [ABSTRACT FROM AUTHOR]

Published
2025
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12. Bacteria induce skin regeneration via IL-1β signaling

Author

Wang, Gaofeng, Sweren, Evan, Liu, Haiyun, Wier, Eric, Alphonse, Martin P., Chen, Ruosi, Islam, Nasif, Li, Ang, Xue, Yingchao, Chen, Junjie, Park, Seungman, Chen, Yun, Lee, Sam, Wang, Yu, Wang, Saifeng, Archer, Nate K., Andrews, William, Kane, Maureen A., Dare, Erika, Reddy, Sashank K., Hu, Zhiqi, Grice, Elizabeth A., Miller, Lloyd S., and Garza, Luis A.

Published
2021
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14. Transcriptomic analysis of atopic dermatitis in African Americans is characterized by Th2/Th17-centered cutaneous immune activation

Author

Wongvibulsin, Shannon, Sutaria, Nishadh, Kannan, Suraj, Alphonse, Martin Prince, Belzberg, Micah, Williams, Kyle A., Brown, Isabelle D., Choi, Justin, Roh, Youkyung Sophie, Pritchard, Thomas, Khanna, Raveena, Eseonu, Amarachi C., Jedrych, Jaroslaw, Dillen, Carly, Kwatra, Madan M., Chien, Anna L., Archer, Nathan, Garza, Luis A., Dong, Xinzhong, Kang, Sewon, and Kwatra, Shawn G.

Published
2021
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15. Preclinical Models and Methodologies for Monitoring Staphylococcus aureus Infections Using Noninvasive Optical Imaging

Author

Archer, Nathan K., primary, Wang, Yu, additional, Ortines, Roger V., additional, Liu, Haiyun, additional, Nolan, Sabrina J., additional, Liu, Qi, additional, Alphonse, Martin P., additional, Dikeman, Dustin A., additional, Mazhar, Momina, additional, Miller, Robert J., additional, Anderson, Leif S., additional, Francis, Kevin P., additional, Simon, Scott I., additional, and Miller, Lloyd S., additional

Published
2019
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17. TNF receptors orchestrate differential neutrophil responses critical to immunity against Staphylococcus aureusskin infection

Author

Youn, Christine, primary, Pontaza, Cristina, additional, Wang, Yu, additional, Dikeman, Dustin A, additional, Joyce, Daniel P, additional, Alphonse, Martin P, additional, Nolan, Sabrina J, additional, Ahmadi, Michael, additional, Young, Jeremy, additional, Tocaj, Aron, additional, Garza, Luis A, additional, Miller, Lloyd S, additional, and Archer, Nathan K, additional

Published
2023
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19. Commensal microbiome promotes hair follicle regeneration by inducing keratinocyte HIF-1α signaling and glutamine metabolism

Author

Wang, Gaofeng, primary, Sweren, Evan, additional, Andrews, William, additional, Li, Yue, additional, Chen, Junjun, additional, Xue, Yingchao, additional, Wier, Eric, additional, Alphonse, Martin P., additional, Luo, Li, additional, Miao, Yong, additional, Chen, Ruosi, additional, Zeng, Dongqiang, additional, Lee, Sam, additional, Li, Ang, additional, Dare, Erika, additional, Kim, Dongwon, additional, Archer, Nathan K., additional, Reddy, Sashank K., additional, Resar, Linda, additional, Hu, Zhiqi, additional, Grice, Elizabeth A., additional, Kane, Maureen A., additional, and Garza, Luis A., additional

Published
2023
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20. Extracellular matrix and dermal nerve growth factor dysregulation in prurigo nodularis compared to atopic dermatitis

Author

Deng, Junwen, primary, Parthasarathy, Varsha, additional, Marani, Melika, additional, Bordeaux, Zachary, additional, Lee, Kevin, additional, Trinh, Chi, additional, Cornman, Hannah L., additional, Kambala, Anusha, additional, Pritchard, Thomas, additional, Chen, Shihua, additional, Sutaria, Nishadh, additional, Oladipo, Olusola O., additional, Kwatra, Madan M., additional, Alphonse, Martin P., additional, and Kwatra, Shawn G., additional

Published
2022
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22. Circulating plasma IL-13 and periostin are dysregulated type 2 inflammatory biomarkers in prurigo nodularis: A cluster analysis

Author

Parthasarathy, Varsha, primary, Cravero, Karen, additional, Deng, Junwen, additional, Sun, Zhe, additional, Engle, Sarah M., additional, Auxier, Autum N., additional, Hahn, Nathan, additional, Sims, Jonathan T., additional, Okragly, Angela J., additional, Alphonse, Martin P., additional, and Kwatra, Shawn G., additional

Published
2022
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23. Topical GZ21T inhibits the growth of actinic keratoses in a UVB induced model of skin carcinogenesis

Author

Bordeaux, Zachary A., primary, Choi, Justin, additional, Braun, Gabriella, additional, Davis, Cole, additional, Marani, Melika, additional, Lee, Kevin, additional, Samuel, Christeen, additional, Adams, Jackson, additional, Windom, Reed, additional, Pollizzi, Anthony, additional, Kambala, Anusha, additional, Cornman, Hannah, additional, Reddy, Sriya V., additional, Lu, Weiying, additional, Oladipo, Olusola O., additional, Alphonse, Martin P., additional, West, Cameron E., additional, Kwatra, Shawn G., additional, and Kwatra, Madan M., additional

Published
2022
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24. GZ17-6.02 Inhibits the Growth of EGFRvIII+ Glioblastoma

Author

Choi, Justin, primary, Bordeaux, Zachary A., additional, McKeel, Jaimie, additional, Nanni, Cory, additional, Sutaria, Nishadh, additional, Braun, Gabriella, additional, Davis, Cole, additional, Miller, Meghan N., additional, Alphonse, Martin P., additional, Kwatra, Shawn G., additional, West, Cameron E., additional, and Kwatra, Madan M., additional

Published
2022
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25. Crisaborole efficacy in murine models of skin inflammation and Staphylococcus aureus infection.

Author

Youn, Christine, Dikeman, Dustin A., Chang, Evelyn, Liu, Haiyun, Nolan, Sabrina J., Alphonse, Martin P., Joyce, Daniel P., Liu, Qi, Meixiong, James, Dong, Xinzhong, Miller, Lloyd S., and Archer, Nathan K.

Subjects
STAPHYLOCOCCUS aureus infections, SKIN inflammation, ITCHING, BACTERIAL colonies, ATOPIC dermatitis, SKIN diseases
Abstract

Phosphodiesterase 4 (PDE4) is highly expressed in keratinocytes and immune cells and promotes pro‐inflammatory responses upon activation. The activity of PDE4 has been attributed to various inflammatory conditions, leading to the development and approval of PDE4 inhibitors as host‐directed therapeutics in humans. For example, the topical PDE4 inhibitor, crisaborole, is approved for the treatment of mild‐to‐moderate atopic dermatitis and has shown efficacy in patients with psoriasis. However, the role of crisaborole in regulating the immunopathogenesis of inflammatory skin diseases and infection is not entirely known. Therefore, we evaluated the effects of crisaborole in multiple mouse models, including psoriasis‐like dermatitis, AD‐like skin inflammation with and without filaggrin mutations, and Staphylococcus aureus skin infection. We discovered that crisaborole dampens myeloid cells and itch in the skin during psoriasis‐like dermatitis. Furthermore, crisaborole was effective in reducing skin inflammation in the context of filaggrin deficiency. Importantly, crisaborole reduced S. aureus skin colonization during AD‐like skin inflammation. However, crisaborole was not efficacious in treating S. aureus skin infections, even as adjunctive therapy to antibiotics. Taken together, we found that crisaborole reduced itch during psoriasis‐like dermatitis and decreased S. aureus skin colonization upon AD‐like skin inflammation, which act as additional mechanisms by which crisaborole dampens the immunopathogenesis in mouse models of inflammatory skin diseases. Further examination is warranted to translate these preclinical findings to human disease. [ABSTRACT FROM AUTHOR]

Published
2023
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26. Dendritic cell immunoreceptor drives atopic dermatitis by modulating oxidized CaMKII-involved mast cell activation

Author

Luo, Xiaoyan, primary, Chen, Jingsi, additional, Yang, Huan, additional, Hu, Xinyue, additional, Alphonse, Martin P., additional, Shen, Yingchun, additional, Kawakami, Yuko, additional, Zhou, Xiaoying, additional, Tu, Wei, additional, Kawakami, Toshiaki, additional, Wan, Mei, additional, Archer, Nathan K., additional, Wang, Hua, additional, and Gao, Peisong, additional

Published
2022
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28. Neutrophil extracellular traps impair regeneration

Author

Wier, Eric, primary, Asada, Mayumi, additional, Wang, Gaofeng, additional, Alphonse, Martin P., additional, Li, Ang, additional, Hintelmann, Chase, additional, Sweren, Evan, additional, Youn, Christine, additional, Pielstick, Brittany, additional, Ortines, Roger, additional, Lyu, Chenyi, additional, Daskam, Maria, additional, Miller, Lloyd S., additional, Archer, Nathan K., additional, and Garza, Luis A., additional

Published
2021
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29. Pan-caspase inhibition as a potential host-directed immunotherapy against MRSA and other bacterial skin infections

Author

Alphonse, Martin P., primary, Rubens, Jessica H., additional, Ortines, Roger V., additional, Orlando, Nicholas A., additional, Patel, Aman M., additional, Dikeman, Dustin, additional, Wang, Yu, additional, Vuong, Ivan, additional, Joyce, Daniel P., additional, Zhang, Jeffrey, additional, Mumtaz, Mohammed, additional, Liu, Haiyun, additional, Liu, Qi, additional, Youn, Christine, additional, Patrick, Garrett J., additional, Ravipati, Advaitaa, additional, Miller, Robert J., additional, Archer, Nathan K., additional, and Miller, Lloyd S., additional

Published
2021
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30. CCR2 contributes to host defense against Staphylococcus aureus orthopedic implant‐associated infections in mice

Author

Wang, Yu, primary, Dikeman, Dustin, additional, Zhang, Jeffrey, additional, Ackerman, Nicole, additional, Kim, Sophia, additional, Alphonse, Martin P., additional, Ortines, Roger V., additional, Liu, Haiyun, additional, Joyce, Daniel P., additional, Dillen, Carly A., additional, Thompson, John M., additional, Thomas, Abigail A., additional, Plaut, Roger D., additional, Miller, Lloyd S., additional, and Archer, Nathan K., additional

Published
2021
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32. Neutrophil-Specific Defensin Receptors Prevent Skin Dysbiosis and Bacterial Infection

Author

Dong, Xintong, primary, Limjunyawong, Nathachit, additional, Sypek, Elizabeth, additional, Wang, Gaofeng, additional, Ortines, Roger, additional, Youn, Christine, additional, Alphonse, Martin P., additional, Dikeman, Dustin, additional, Wang, Yu, additional, Lay, Mark, additional, Pundir, Priyanka, additional, Goff, Loyal, additional, Miller, Lloyd S., additional, Lu, Wuyuan, additional, Garza, Luis, additional, Kim, Brian S., additional, Archer, Nate K., additional, and Dong, Xinzhong, additional

Published
2021
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33. Neutrophil extracellular traps impair regeneration

Author

Wier, Eric, primary, Asada, Mayumi, additional, Wang, Gaofeng, additional, Alphonse, Martin P., additional, Li, Ang, additional, Hintelmann, Chase, additional, Youn, Christine, additional, Pielstick, Brittany, additional, Ortines, Roger, additional, Miller, Lloyd S., additional, Archer, Nathan K., additional, and Garza, Luis A., additional

Published
2020
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34. CCR2 contributes to host defense against Staphylococcus aureus orthopedic implant‐associated infections in mice.

Author

Wang, Yu, Dikeman, Dustin, Zhang, Jeffrey, Ackerman, Nicole, Kim, Sophia, Alphonse, Martin P., Ortines, Roger V., Liu, Haiyun, Joyce, Daniel P., Dillen, Carly A., Thompson, John M., Thomas, Abigail A., Plaut, Roger D., Miller, Lloyd S., and Archer, Nathan K.

Subjects
CHEMOKINE receptors, STAPHYLOCOCCUS aureus, LYSIS, MYELOID cells, MICE
Abstract

C‐C motif chemokine receptor 2 (CCR2) is an important mediator of myeloid cell chemotaxis during inflammation and infection. Myeloid cells such as monocytes, macrophages, and neutrophils contribute to host defense during orthopedic implant‐associated infections (OIAI), but whether CCR2‐mediated chemotaxis is involved remains unclear. Therefore, a Staphylococcus aureus OIAI model was performed by surgically placing an orthopedic‐grade titanium implant and inoculating a bioluminescent S. aureus strain in knee joints of wildtype (wt) and CCR2‐deficient mice. In vivo bioluminescent signals significantly increased in CCR2‐deficient mice compared with wt mice at later time points (Days 14–28), which was confirmed with ex vivo colony‐forming unit enumeration. S. aureus γ‐hemolysin utilizes CCR2 to induce host cell lysis. However, there were no differences in bacterial burden when the OIAI model was performed with a parental versus a mutant γ‐hemolysin‐deficient S. aureus strain, indicating that the protection was mediated by the host cell function of CCR2 rather than γ‐hemolysin virulence. Although CCR2‐deficient and wt mice had similar cellular infiltrates in the infected joint tissue, CCR2‐deficient mice had reduced myeloid cells and γδ T cells in the draining lymph nodes. Taken together, CCR2 contributed to host defense at later time points during an OIAI by increasing immune cell infiltrates in the draining lymph nodes, which likely contained the infection and prevented invasive spread. [ABSTRACT FROM AUTHOR]

Published
2022
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35. Cutaneous Transcriptomics Identifies Fibroproliferative and Neurovascular Gene Dysregulation in Prurigo Nodularis Compared with Psoriasis and Atopic Dermatitis

Author

Sutaria, Nishadh, Alphonse, Martin Prince, Roh, Youkyung S., Choi, Justin, Parthasarathy, Varsha, Deng, Junwen, Bordeaux, Zachary A., Taylor, Matthew T., Pritchard, Thomas, Kim, Noori, Aguh, Crystal, Semenov, Yevgeniy R., Archer, Nathan K., Garza, Luis A., Kang, Sewon, and Kwatra, Shawn G.

Published
2022
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36. Bacteria Induce Skin Regeneration Via Il-1β Signaling

Author

Wang, Gaofeng, primary, Liu, Haiyun, additional, Sweren, Evan, additional, Wier, Eric, additional, Alphonse, Martin P., additional, Islam, Nasif, additional, Li, Ang, additional, Xue, Yingchao, additional, Lee, Sam, additional, Wang, Yu, additional, Archer, Nate K., additional, Hu, Zhiqi, additional, Grice, Elizabeth A., additional, Miller, Lloyd S., additional, and Garza, Luis, additional

Published
2020
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37. The Viral Defense Gene RNaseL Acts as a Regeneration Repressor

Author

Islam, Nasif, primary, Wier, Eric, additional, Alphonse, Martin P., additional, Liu, Haiyun, additional, Kim, Dongwon, additional, Li, Ang, additional, Reddy, Sashank, additional, Miller, Lloyd S., additional, Yu, Jianshi, additional, Huang, Weiliang, additional, Jones, Jace W., additional, Lee, Sam, additional, Kim, Sooah, additional, Wang, Gaofeng, additional, Hintelmann, Chase, additional, Sheu, Mary, additional, Kim, Noori, additional, Kang, Sewon, additional, Kane, Maureen A., additional, Silverman, Robert H., additional, and Garza, Luis, additional

Published
2020
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39. Clonal Vγ6 + Vδ4 + T cells promote IL-17–mediated immunity against Staphylococcus aureus skin infection

Author

Marchitto, Mark C., primary, Dillen, Carly A., additional, Liu, Haiyun, additional, Miller, Robert J., additional, Archer, Nathan K., additional, Ortines, Roger V., additional, Alphonse, Martin P., additional, Marusina, Alina I., additional, Merleev, Alexander A., additional, Wang, Yu, additional, Pinsker, Bret L., additional, Byrd, Angel S., additional, Brown, Isabelle D., additional, Ravipati, Advaitaa, additional, Zhang, Emily, additional, Cai, Shuting S., additional, Limjunyawong, Nathachit, additional, Dong, Xinzhong, additional, Yeaman, Michael R., additional, Simon, Scott I., additional, Shen, Wei, additional, Durum, Scott K., additional, O’Brien, Rebecca L., additional, Maverakis, Emanual, additional, and Miller, Lloyd S., additional

Published
2019
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Author

Marchitto, Mark C, Marchitto, Mark C, Dillen, Carly A, Liu, Haiyun, Miller, Robert J, Archer, Nathan K, Ortines, Roger V, Alphonse, Martin P, Marusina, Alina I, Merleev, Alexander A, Wang, Yu, Pinsker, Bret L, Byrd, Angel S, Brown, Isabelle D, Ravipati, Advaitaa, Zhang, Emily, Cai, Shuting S, Limjunyawong, Nathachit, Dong, Xinzhong, Yeaman, Michael R, Simon, Scott I, Shen, Wei, Durum, Scott K, O’Brien, Rebecca L, Maverakis, Emanual, Miller, Lloyd S, Marchitto, Mark C, Marchitto, Mark C, Dillen, Carly A, Liu, Haiyun, Miller, Robert J, Archer, Nathan K, Ortines, Roger V, Alphonse, Martin P, Marusina, Alina I, Merleev, Alexander A, Wang, Yu, Pinsker, Bret L, Byrd, Angel S, Brown, Isabelle D, Ravipati, Advaitaa, Zhang, Emily, Cai, Shuting S, Limjunyawong, Nathachit, Dong, Xinzhong, Yeaman, Michael R, Simon, Scott I, Shen, Wei, Durum, Scott K, O’Brien, Rebecca L, Maverakis, Emanual, and Miller, Lloyd S

Published
2019

42. Genetic Variation in the SLC8A1 Calcium Signaling Pathway Is Associated With Susceptibility to Kawasaki Disease and Coronary Artery Abnormalities

Author

Shimizu, Chisato, Eleftherohorinou, Hariklia, Wright, Victoria J, Kim, Jihoon, Alphonse, Martin P, Perry, James C, Cimaz, Rolando, Burgner, David, Dahdah, Nagib, Hoang, Long T, Khor, Chiea Chuen, Salgado, Andrea, Tremoulet, Adriana H, Davila, Sonia, Kuijpers, Taco W, Hibberd, Martin L, Johnson, Todd A, Takahashi, Atsushi, Tsunoda, Tatsuhiko, Kubo, Michiaki, Tanaka, Toshihiro, Onouchi, Yoshihiro, Yeung, Rae SM, Coin, Lachlan JM, Levin, Michael, Burns, Jane C, and International Kawasaki Disease Genetics Consortium

Abstract

BACKGROUND: Kawasaki disease (KD) is an acute pediatric vasculitis in which host genetics influence both susceptibility to KD and the formation of coronary artery aneurysms. Variants discovered by genome-wide association studies and linkage studies only partially explain the influence of genetics on KD susceptibility. METHODS AND RESULTS: To search for additional functional genetic variation, we performed pathway and gene stability analysis on a genome-wide association study data set. Pathway analysis using European genome-wide association study data identified 100 significantly associated pathways (P

Published
2016

43. Clonal Vγ6+Vδ4+ T cells promote IL-17-mediated immunity against Staphylococcus aureus skin infection.

Author

Maverakis, Emanual, Marchitto, Mark C., Dillen, Carly A., Haiyun Liu, Miller, Robert J., Archer, Nathan K., Ortines, Roger V., Alphonse, Martin P., Yu Wang, Pinsker, Bret L., Byrd, Angel S., Brown, Isabelle D., Ravipati, Advaitaa, Zhang, Emily, Cai, Shuting S., Simon, Scott I., Wei Shen, Durum, Scott K., O'Brien, Rebecca L., and Millera, Lloyd S.

Subjects
STAPHYLOCOCCUS aureus infections, T cells, IMMUNITY, SKIN infections, INTERLEUKIN-17, ANTIBIOTICS, LYMPH nodes, NEUTROPHILS
Abstract

T cell cytokines contribute to immunity against Staphylococcus aureus, but the predominant T cell subsets involved are unclear. In an S. aureus skin infection mouse model, we found that the IL- 17 response was mediated by γδ T cells, which trafficked from lymph nodes to the infected skin to induce neutrophil recruitment, proinflammatory cytokines IL-1α, IL-1β, and TNF, and host defense peptides. RNA-seq for TRG and TRD sequences in lymph nodes and skin revealed a single clonotypic expansion of the encoded complementarity-determining region 3 amino acid sequence, which could be generated by canonical nucleotide sequences of TRGV5 or TRGV6 and TRDV4. However, only TRGV6 and TRDV4 but not TRGV5 sequences expanded. Finally, Vγ6+ T cells were a predominant γδ T cell subset that produced IL-17A as well as IL-22, TNF, and IFNγ, indicating a broad and substantial role for clonal Vγ6+Vδ4+ T cells in immunity against S. aureus skin infections. [ABSTRACT FROM AUTHOR]

Published
2019
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44. Genetic Variation in the SLC8A1 Calcium Signaling Pathway Is Associated With Susceptibility to Kawasaki Disease and Coronary Artery Abnormalities

Author

Shimizu, Chisato, primary, Eleftherohorinou, Hariklia, additional, Wright, Victoria J., additional, Kim, Jihoon, additional, Alphonse, Martin P., additional, Perry, James C., additional, Cimaz, Rolando, additional, Burgner, David, additional, Dahdah, Nagib, additional, Hoang, Long T., additional, Khor, Chiea Chuen, additional, Salgado, Andrea, additional, Tremoulet, Adriana H., additional, Davila, Sonia, additional, Kuijpers, Taco W., additional, Hibberd, Martin L., additional, Johnson, Todd A., additional, Takahashi, Atsushi, additional, Tsunoda, Tatsuhiko, additional, Kubo, Michiaki, additional, Tanaka, Toshihiro, additional, Onouchi, Yoshihiro, additional, Yeung, Rae S.M., additional, Coin, Lachlan J.M., additional, Levin, Michael, additional, and Burns, Jane C., additional

Published
2016
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45. A Polygenic Risk Score for Predicting Racial and Genetic Susceptibility to Prurigo Nodularis

Author

Vasavda, Chirag, Wan, Guihong, Szeto, Mindy D., Marani, Melika, Sutaria, Nishadh, Rajeh, Ahmad, Lu, Chenyue, Lee, Kevin K., Nguyen, Nga T.T., Adawi, Waleed, Deng, Junwen, Parthasarathy, Varsha, Bordeaux, Zachary A., Taylor, Matthew T., Alphonse, Martin P., Kwatra, Madan M., Kang, Sewon, Semenov, Yevgeniy R., Gusev, Alexander, and Kwatra, Shawn G.

Abstract

Prurigo nodularis (PN) is an understudied inflammatory skin disease characterized by pruritic, hyperkeratotic nodules. Identifying the genetic factors underlying PN could help to better understand its etiology and guide the development of therapies. In this study, we developed a polygenic risk score that predicts a diagnosis of PN (OR = 1.41, P = 1.6 × 10−5) in two independent and continentally distinct populations. We also performed GWASs, which uncovered genetic variants associated with PN, including one near PLCB4(rs6039266: OR = 3.15, P = 4.8 × 10−8) and others near TXNRD1(rs34217906: OR = 1.71, P = 6.4 × 10−7; rs7134193: OR = 1.57, P = 1.1 × 10−6). Finally, we discovered that Black patients have over a two-times greater genetic risk of developing PN (OR = 2.63, P = 7.8 × 10−4). Combining the polygenic risk score and self-reported race together was significantly predictive of PN (OR = 1.32, P = 4.7 × 10−3). Strikingly, this association was more significant with race than after adjusting for genetic ancestry. Because race is a sociocultural construct and not a genetically bound category, our findings suggest that genetics, environmental influence, and social determinants of health likely affect the development of PN and may contribute to clinically observed racial disparities.

Published
2024
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46. Abstract O.21: Inositol 1,4,5 triphosphate 3- kinase C regulates NLRP3 Inflammasome activation in Kawasaki disease

Author

Alphonse, Martin P, primary, Duong, Trang T, additional, Shimizu, Chisato, additional, Hoang, Long T, additional, McCrindle, Brian W, additional, Franco, Alessandra, additional, Schurmans, Stephane, additional, Philpott, Dana J, additional, Hibberd, Martin L, additional, Burns, Jane C, additional, Kuijpers, Taco W, additional, and Yeung, Rae S, additional

Published
2015
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49. Cutaneous Toxicities Associated with Immune Checkpoint Inhibitors: An Observational, Pharmacovigilance Study

Author

Le, Thomas K., Brown, Isabelle, Goldberg, Rebecca, Taylor, Matthew T., Deng, Junwen, Parthasarathy, Varsha, Bordeaux, Zachary A., Alphonse, Martin Prince, Kwatra, Madan M., Naranbhai, Vivek, Gusev, Alexander, Alhariri, Jihad, LeBoeuf, Nicole R., Reynolds, Kerry L., Cappelli, Laura C., Naidoo, Jarushka, Brahmer, Julie R., Kang, Sewon, Semenov, Yevgeniy R., and Kwatra, Shawn G.

Abstract

Cutaneous immune-related adverse events (cirAEs) are the most prevalent complication to arise from immunotherapy and cause significant morbidity. We aimed to determine the spectrum, timing, clinical features, and outcomes of cirAEs by conducting an observational pharmacovigilance study using VigiBase, the World Health Organization’s global database of individual case safety reports from over 130 member countries (ClinicalTrials.gov, number NCT04898751).We compared adverse event reporting in patients who received immune checkpoint inhibitors (91,323 adverse events) with those of the full reporting database (18,919,358 adverse events). There were 10,933 cases of cirAEs within 51 distinct dermatologic types, with 27 specific eruptions with disproportionate signal represented (information component [IC]025> 0). Of these 27 eruptions, there were eight cirAEs with n > 100 reports, including vitiligo (IC025 = 4.87), bullous pemphigoid (IC025 = 4.08), lichenoid dermatitis (IC025 = 3.69), erythema multiforme (IC025 = 1.03), toxic epidermal necrolysis (IC025 = 0.95), Stevens‒Johnson syndrome (IC025 = 0.41), drug eruption (IC025 = 0.11), and eczematous dermatitis (IC025 = 0.11). There were differences in time to onset after immune checkpoint inhibitor initiation, with a median of approximately 1 month (erythema multiforme, Stevens‒Johnson syndrome, and toxic epidermal necrolysis), 2 months (drug eruption and eczematous dermatitis), 4 months (lichenoid dermatitis), and 5‒6 months (bullous pemphigoid and vitiligo). CirAEs are diverse, dependent on cancer type, and have distinct and different onset times that are linked to the cirAE subtype.

Published
2022
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50. Cluster Analysis of Circulating Plasma Biomarkers in Prurigo Nodularis Reveals a Distinct Systemic Inflammatory Signature in African Americans

Author

Sutaria, Nishadh, Alphonse, Martin Prince, Marani, Melika, Parthasarathy, Varsha, Deng, Junwen, Wongvibulsin, Shannon, Williams, Kyle, Roh, Youkyung Sophie, Choi, Justin, Bordeaux, Zachary, Pritchard, Thomas, Dillen, Carly, Semenov, Yevgeniy R., Kwatra, Madan M., Archer, Nathan K., Garza, Luis A., Dong, Xinzhong, Kang, Sewon, and Kwatra, Shawn G.

Abstract

Patients with prurigo nodularis (PN) suffer from intractable itch and dramatic reduction in QOL. Although there is significant clinical heterogeneity in the presentation of PN, disease endotypes remain unknown. We assayed circulating plasma cytokine concentrations in patients with PN (n = 20) along with matched healthy controls and utilized an unsupervised machine learning algorithm to identify disease endotypes. We found two distinct clusters of patients with PN with noninflammatory (cluster 1) and inflammatory (cluster 2) plasma profiles. Cluster 2 had more African Americans (82%, n = 9 vs. 33%, n = 3; P = 0.028), higher Worst Itch Numeric Rating Scale scores (9.5 ± 0.9 vs. 8.3 ± 1.2; P = 0.036), and lower QOL as reflected by higher Dermatology Life Quality Index scores (21.9 ± 6.4 vs. 13.0 ± 4.1; P = 0.015). In addition, cluster 1 had a higher rate of myelopathy (67%, n = 6 vs. 18%, n = 2; P = 0.028). Compared with cluster 1, cluster 2 had higher levels of IL-1α, IL-4, IL-5, IL-6, IL-10, IL-17A, IL-22, IL-25, and IFN-α. With population-level analysis, African American patients with PN had higher erythrocyte sedimentation rate, C-reactive protein, ferritin, and eosinophils and lower transferrin than Caucasian patients with PN. These findings indicate discrete clusters of patients with PN with plasma biomarker profiles corresponding to distinct demographic and clinical characteristics, potentially allowing for precision medicine approaches to treat PN.

Published
2022
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