Search

Your search keyword '"Kloepfer, Kirsten M."' showing total 42 results
Start Over Author "Kloepfer, Kirsten M." Language english
42 results on '"Kloepfer, Kirsten M."'

4. The Precision Interventions for Severe and/or Exacerbation-Prone (PrecISE) Asthma Network: An overview of Network organization, procedures, and interventions

Author

Billheimer, Dean, Bleecker, Eugene R., Branch, Emily, Conway, Michelle, Daines, Cori, Deaton, Isaac, Evans, Alexandria, Field, Paige, Francisco, Dave, Hastie, Annette T., Hmieleski, Bob, Krings, Jeffrey O., Liu, Yanqin, Merchen, Janell L., Meyers, Deborah A., Narendran, Nirushan, Peters, Stephen P., Pippins, Anna, Rank, Matthew A., Schunk, Ronald, Skeps, Raymond, Wright, Benjamin, Banzon, Tina M., Bartnikas, Lisa M., Baxi, Sachin N., Betapudi, Vishwanath, Brick, Isabelle, Brockway, Conor, Casale, Thomas B., Castillo-Ruano, Kathleen, Cinelli, Maria Angeles, Crestani, Elena, Cunningham, Amparito, Day-Lewis, Megan, Diaz-Cabrera, Natalie, DiMango, Angela, Esty, Brittany, Fandozzi, Eva, Fernandez, Jesse, Fitzpatrick, Elizabeth, Forth, Victoria E., Gentile, Katarina, Gubernick, David, Gueye-Ndiaye, Seyni, Gunnlaagsson, Sigfus, Hauptmann, Marissa, Hudey, Stephanie N., Imanirad, Donya S., Kaage, Tiffani, Kolinsky, Nicholas, LaBere, Brenna, Lai, Peggy Sue, Le, Meghan, Ledford, Dennis K., Lockey, Richard, Louisias, Margee, Macginnitie, Andrew J., Maciag, Michelle C., O’Neill, Allison, Pepper, Amber N., Permaul, Perdita, Pugh, Mya, Queheillalt, Dianna, Saroya, Tarnjot, Sheehan, William, Smith, Catherine, Socolovsky, Carmela, Treffeisen, Else, Trippa, Lorenzo, Tulchinsky, Abigail, Yee, Christina, Carter, Tina, Fu, Jun, Garcia, Vanessa, Hixon, Jenny, Jackson, Carly, Ji, Yuan, Kalhan, Ravi, Kaur, Opinderjit, Li, Grace, Makhija, Melanie M., Maleckar, Spring, Naureckas, Edward T., Peters, Anju T., Press, Valerie, Qureshi, Mehreen, Reyfman, Paul A., Rosenberg, Sharon R., Ryba, Dominika, Sheng, Jianrong, Xu, Ben, Alam, Rafeul, Anderson, Darci, Belimezova, Sonya, Bitzan, Jennifer, Chupp, Geoffrey, Clark, Brian J., Cohn, Lauren, Cruse, Margaret Hope, Estrom, Jean, Freid, Leah, Villalobos, Jose Gomez, Grant, Nicole, Guntur, Vamsi P., Holm, Carole, Kolakowski, Christena, Manka, Laurie A., Miyazawa, Naomi, Pak, Juno, Pruitt, Diana M., Sharma, Sunita, Stevens, Allen D., Thomas, Kisori, Tippin, Brooke, Valente, Karissa, Wainscoat, Cynthia L., White, Michael P., Winnica, Daniel, Ye, Shuyu, Zeitlin, Pamela L., Bach, Julia, Brownell, Joshua, Castro, Lauren, DeLisa, Julie, Fain, Sean B., Fichtinger, Paul S., Floerke, Heather, Gern, James E., Goswamy, Vinay, Grogan, Jenelle, Hasse, Wendy, Kelley, Rick L., Klaus, Danika, LaBedz, Stephanie, Lowell, Paige, Maddox, Andrew, Mathur, Sameer K., McIntyre, Amanda, Norwick, Lourdes M., Nyenhuis, Sharmilee M., O’Brien, Matthew J., Palas, Tina, Pappalardo, Andrea A., Potter, Mark, Ramratnam, Sima K., Rosenberg, Daniel L., Schauberger, Eric M., Schiebler, Mark L., Schraml, Angela, Sorkness, Ronald L., Taki, Mohamed, Tattersall, Matthew C., Torres, Jissell, Wollet, Lori, Abi-Saleh, Simon, Bendy, Lisa, Borish, Larry, Chmiel, James F., Dix, Aska, France, Lisa, Gammell, Rebecca, Gluvna, Adam, Hirth, Brittany, Hu, Bo, Hyser, Elise, Kloepfer, Kirsten M., Koo, Michelle, Krupp, Nadia L., Labadia, Monica, Lawrence, Joy, Logan, Laurie, Marko, Angela, Matuska, Brittany, Murphy, Deborah, Owensby, Rachel, Roesch, Erica A., Sanders, Don B., Sharp, Jackie, Teague, W. Gerald, Veri, Laura, Shifflett, Kristin Wavell, Camiolo, Matt, Collins, Sarah, Demas, Jessa, Elvin, Courtney, Gauthier, Marc C., Ilnicki, Melissa, Ingram, Jenn, Lane, Lisa, Nouraie, Seyed Mehdi, Trudeau, John B., Zhang, Michael, Barry, Jeffrey, Brickner, Howard, Celso, Janelle, Cernelc-Kohan, Matejka, Diaz, Damaris, Du, Ashley, Jain, Sonia, Liu, Neiman, Nazir, Yusife, Ryu, Julie, Vijayanand, Pandurangan, Almario, Rogelio, Baum, Ariana, Brown, Kellen, Chan, Marilynn H., Gale, Barbara, Haczku, Angela, Harper, Richart W., Heromin, Raymond, Kivler, Celeste, Kuhn, Brooks T., Ly, Ngoc P., McCourt, Paula, Orain, Xavier, Plough, Audrey, Ramirez, Karla, Roberts, Ellese, Schivo, Michael, Singapuri, Amisha, Tham, Tina, Tompkins, Daniel, Twitmyer, Patricia Michelle, Vi, Jade, Atha, Jarron, Bedard, Jennifer, Boomer, Jonathan S., Chung, Andrew, Curtis, Vanessa, Hall, Chase S., Hart, Emily, Jackson, Fatima, Kemp, Pamela, Maxwell, Sharli, Messplay, Maggie, Ramirez, Crystal, Thompson, Brynne, Britt, Ashley, Bryan, Hope, Gotman, Nathan M., Jiang, Yue, Kosorok, Michael R., Mauger, David T., Meekins, Kelsey, Mollenhauer, Jeanette K., Moody, Sarah, Ritz, Cheyanne, Schwartz, Stefanie, Thomlinson, Chalmer, Wilson, Nicole, Georas, Steve N., Wright, Rosalind J., Ivanova, Anastasia, Israel, Elliot, LaVange, Lisa M., Akuthota, Praveen, Carr, Tara F., Denlinger, Loren C., Fajt, Merritt L., Kumar, Rajesh, O’Neal, Wanda K., Phipatanakul, Wanda, Szefler, Stanley J., Aronica, Mark A., Bacharier, Leonard B., Burbank, Allison J., Castro, Mario, Crotty Alexander, Laura, Bamdad, Julie, Cardet, Juan Carlos, Comhair, Suzy A.A., Covar, Ronina A., DiMango, Emily A., Erwin, Kim, Erzurum, Serpil C., Fahy, John V., Gaffin, Jonathan M., Gaston, Benjamin, Gerald, Lynn B., Hoffman, Eric A., Holguin, Fernando, Jackson, Daniel J., James, John, Jarjour, Nizar N., Kenyon, Nicholas J., Khatri, Sumita, Kirwan, John P., Kraft, Monica, Krishnan, Jerry A., Liu, Andrew H., Liu, Mark C., Marquis, M. Alison, Martinez, Fernando, Mey, Jacob, Moore, Wendy C., Moy, James N., Ortega, Victor E., Peden, David B., Pennington, Emily, Peters, Michael C., Ross, Kristie, Sanchez, Maria, Smith, Lewis J., Wechsler, Michael E., Wenzel, Sally E., White, Steven R., Zein, Joe, Zeki, Amir A., and Noel, Patricia

Published
2022
Full Text
View/download PDF

6. Preventing asthma in high risk kids (PARK) with omalizumab: Design, rationale, methods, lessons learned and adaptation

Author

Bartnikas, Lisa, Kantor, David, Permaul, Perdita, Akar-Ghibril, Nicole, Haktanir-Abul, Mehtap, Gunnalaugsson, Sigfus, Esty, Brittany, Crestani, Elena, Maciag, Michelle, Hauptman, Marissa, Baxi, Sachin N., Burke-Roberts, Elizabeth, Louisias, Margee, Banzon, Tina, Habiballah, Saddiq, Nguyen, Alan, Simoneau, Tregony, Minnicozzi, Samantha, Treffeisen, Elsa, LaBere, Brenna, Chandler, Mia, Fanny, Manoussa, Vasquez-Muniz, Anna Cristina, Konzelman, Vanessa, Garcia, Giselle, Waskosky, Sullivan, Ramsey, Anna, Ansel-Kelly, Ethan, Fitzpatrick, Elizabeth, Bairaktaris, Vaia, Fernandez, Jesse, Hollister, Brianna, Lewis, Owen, McIntosh, Masai, Almeida, Sigrid, Kercsmar, Carolyn, McDowell, Karen, Shipp, Cassie, Ward, Stephanie (Logsdon), Lin, Nancy, George, Alisha, Simpson, Ryne, St. Onge, Ina, Corwin, Will, Geigle, Grant, Hartmann, Alisha, Broderick, John, Szefler, Stanley, Miyazawa, Naomi, Tippin, Brooke, Anderson, Darci, Belimezova, Sonya, Navanandan, Nidhya, Watson, Tanya, Olson, Michelle, Caldwell, Wanda, Horner, Caroline, Kertz, Lila, Norris, Tina, Rivera-Spoljaric, Katherine, Stokes, Jeffrey, Coverstone, Andrea, McDowell, Molly, Laughlin, Sarah, Laury, Gina, Donato, Rosanne, Beckett-Firmage, Elizabeth, Cornidez, Elia A., Lopez, Silvia, Simon, Michele, Skeps, Raymond, Vasquez, Monica, Gage, Rob, Shearer, Heather, Pecak, Melissa, Winters, Sandi, Rukasin, Christine, McNally, Bernadette, Johnson, Darcy, Vickery, Brian, Grunwell, Jocelyn, Nicholls, Morgan, El-Hussein, Taqwa, Patel, Shilpa, Pillai, Dinsesh, Makhija, Melanie, Robison, Rachel, Bosworth, Jennifer, Catalano, Michelle, Cassin, Kathleen, DeLeon, Laura Bamaca, Titus, Nicole, Leibel, Sydney, Aceves, Seema, Mortazavi, Diba, Loop, Lauren, Anvari, Sara, Anagnostou, Aikaterini, Pitts, Kathy, Sebutra, Sopar, Tran, Daisy, McMullen-Jackson, Chivon, Jin, Jay, Krupp, Nadia, Ren, Clement, Vitalpur, Girish, Shively, Lori, Campbell, Patrick, Bendy, Lisa, France, Lisa, Jara, Sylvia, Cichy, Sarah, Engle, Linda, Merchlinski, Aimee, Payton, Melanie, Ramsey, Pam, Schmidt, James, Tekely, Dan, Updegrave, Angela, Weber, Rachel, Zimmerman, Ronald, Jr, Thorne, Peter S., Metwali, Nervana, Jing, Xuefang, Walker, Melissa, Sigelman, Steven S., Li, Ling, Hamrah, Sanaz, Phipatanakul, Wanda, Mauger, David T., Guilbert, Theresa W., Bacharier, Leonard B., Durrani, Sandy, Jackson, Daniel J., Martinez, Fernando D., Fitzpatrick, Anne M., Cunningham, Amparito, Kunselman, Susan, Wheatley, Lisa M., Bauer, Cindy, Davis, Carla M., Geng, Bob, Kloepfer, Kirsten M., Lapin, Craig, Liu, Andrew H., Pongracic, Jacqueline A., Teach, Stephen J., Chmiel, James, Gaffin, Jonathan M., Greenhawt, Matthew, Gupta, Meera R., Lai, Peggy S., Lemanske, Robert F., Morgan, Wayne J., Sheehan, William J., Oettgen, Hans C., and Israel, Elliot

Published
2021
Full Text
View/download PDF

21. Methods in Lung Microbiome Research.

Author

Carney, Sharon M., Clemente, Jose C., Cox, Michael J., Dickson, Robert P., Huang, Yvonne J., Kitsios, Georgios D., Kloepfer, Kirsten M., Leung, Janice M., LeVan, Tricia D., Molyneaux, Philip L., Moore, Bethany B., O'Dwyer, David N., Segal, Leopoldo N., and Garantziotis, Stavros

Subjects
LUNG microbiology, IMMUNE response, HUMAN microbiota, CONCEPTUAL models, DATA analysis
Abstract

The lung microbiome is associated with host immune response and health outcomes in experimental models and patient cohorts. Lung microbiome research is increasing in volume and scope; however, there are no established guidelines for study design, conduct, and reporting of lung microbiome studies. Standardized approaches to yield reliable and reproducible data that can be synthesized across studies will ultimately improve the scientific rigor and impact of published work and greatly benefit microbiome research. In this review, we identify and address several key elements of microbiome research: conceptual modeling and hypothesis framing; study design; experimental methodology and pitfalls; data analysis; and reporting considerations. Finally, we explore possible future directions and research opportunities. Our goal is to aid investigators who are interested in this burgeoning research area and hopefully provide the foundation for formulating consensus approaches in lung microbiome research. [ABSTRACT FROM AUTHOR]

Published
2020
Full Text
View/download PDF

25. Detection of Pathogenic Bacteria During Rhinovirus Infection is Associated with Increased Respiratory Symptoms and Exacerbations of Asthma

Author

Kloepfer, Kirsten M., Lee, Wai Ming, Pappas, Tressa E., Kang, Teresa, Vrtis, Rose F., Evans, Michael D., Gangnon, Ronald E., Bochkov, Yury A., Jackson, Daniel J., Lemanske, Robert F., and Gern, James E.

Subjects
DNA, Bacterial, Male, Picornaviridae Infections, Bacteria, Rhinovirus, Child, Preschool, Humans, Female, Bacterial Infections, Child, Polymerase Chain Reaction, Article, Asthma
Abstract

Detection of either viral or bacterial pathogens is associated with wheezing in children; however, the influence of both bacteria and viruses on illness symptoms has not been described.We evaluated bacterial detection during the peak rhinovirus season in children with and without asthma to determine whether an association exists between bacterial infection and the severity of rhinovirus-induced illnesses.Three hundred eight children (166 with asthma and 142 without asthma) aged 4 to 12 years provided 5 consecutive weekly nasal samples during September and scored cold and asthma symptoms daily. Viral diagnostics and quantitative PCR for Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis were performed on all nasal samples.Detection rates were 53%, 17%, and 11% for H influenzae, S pneumoniae, and M catarrhalis, respectively, with detection of rhinovirus increasing the risk of detecting bacteria within the same sample (odds ratio [OR], 2.0; 95% CI, 1.4-2.7; P.0001) or the following week (OR, 1.6; 95% CI, 1.1-2.4; P = .02). In the absence of rhinovirus, S pneumoniae was associated with increased cold symptoms (mean, 2.7 [95% CI, 2.0-3.5] vs 1.8 [95% CI, 1.5-2.2]; P = .006) and moderate asthma exacerbations (18% [95% CI, 12% to 27%] vs 9.2% [95% CI, 6.7% to 12%]; P = .006). In the presence of rhinovirus, S pneumoniae was associated with increased moderate asthma exacerbations (22% [95% CI, 16% to 29%] vs 15% [95% CI, 11% to 20%]; P = .01). Furthermore, M catarrhalis detected alongside rhinovirus increased the likelihood of experiencing cold symptoms, asthma symptoms, or both compared with isolated detection of rhinovirus (OR, 2.0 [95% CI, 1.0-4.1]; P = .04). Regardless of rhinovirus status, H influenzae was not associated with respiratory symptoms.Rhinovirus infection enhances detection of specific bacterial pathogens in children with and without asthma. Furthermore, these findings suggest that M catarrhalis and S pneumoniae contribute to the severity of respiratory tract illnesses, including asthma exacerbations.

Published
2014

29. Effects of Montelukast in Subjects With Asthma After Experimental Inoculation with Rhinovirus-16

Author

Kloepfer, Kirsten M., DeMore, Jennifer P., Vrtis, Rose F., Swenson, Cheri A., Gaworski, Katie L., Bork, Jack A., Evans, Michael D., and Gern, James E.

Subjects
Cyclopropanes, Male, Rhinovirus, Reverse Transcriptase Polymerase Chain Reaction, Common Cold, Pilot Projects, Acetates, Sulfides, Article, Asthma, Respiratory Function Tests, Young Adult, Double-Blind Method, Quinolines, Humans, Leukotriene Antagonists, RNA, Viral, Female
Abstract

Leukotrienes are induced by viral infections.To determine whether treatment with montelukast would improve asthma disease control in patients with mild allergic asthma during an experimentally induced rhinovirus infection.Patients with mild allergic asthma were randomized to receive treatment with either montelukast or placebo, and 7 days later both groups were inoculated with human rhinovirus 16. Patients were evaluated at baseline, during the acute infection phase, and during the recovery phase for asthma and cold symptoms by questionnaire. Sputum, nasal lavage fluid, and blood were analyzed for viral shedding and cellular inflammation, and peak expiratory flow was measured daily.A total of 19 patients (11 in the placebo group and 8 in the active group) completed the study. No significant differences were found in asthma control and cold symptom scores between the control and treatment groups. The change in peak expiratory flow from the randomization to acute illness phase was greater in the placebo group than the treatment group (mean, -22 vs 0 L/min; P = .05). During the recovery phase, the percentage of sputum eosinophils increased in the placebo group and remained at baseline levels in the montelukast group (median, 2.7% vs 0.2%; P = .05 between groups).In this pilot study, montelukast did not improve asthma control or cold symptom scores caused by experimental rhinovirus infection. Analysis of secondary outcomes suggests that montelukast may prevent reductions in lung function and increases in sputum eosinophils caused by common cold infections. Further studies are needed to determine whether these effects are associated with clinically significant improvements in health outcomes during natural colds.clinicaltrials.gov Identifier: NCT00359073.

Published
2011

33. Multisystem reactions during egg oral food challenges may be associated with less severe reactions on initial presentation.

Author

Vitalpur, Girish, Esquivel, Ann, Kloepfer, Kirsten M., Slaven, James E., and Leickly, Frederick E.

Subjects
EGGS, FOOD allergy, IMMUNOLOGIC diseases, IMMUNOLOGY
Abstract

In this study, we assessed whether multisystem reactions to egg and extensively-heated (EH) egg during OFCs were associated with a history of multisystem reactions. Records of children, who underwent OFC to egg or EH egg over a five-year period were reviewed. Of the 120 challenges, 26 (21.67 %) failed, with 38.4 % (10/26) having multisystem reactions. Of the 13 who had multisystem reactions on initial presentation, only two (15.4 %) had a similar OFC outcome. Eighty percent (8/10) of those who had a multisystem OFC reaction had a less severe initial presentation. Initial and OFC multisystem reactions were not associated with each other. [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

34. Patient Preferences for Symptom-Driven or Regular Preventer Treatment in Mild to Moderate Asthma: Findings From the PRACTICAL Study, a Randomised Clinical Trial.

Author

Huddleston, Christina M. and Kloepfer, Kirsten M.

Subjects
*ASTHMA prevention, *DRUG therapy for asthma, *ADRENOCORTICAL hormones, *BRONCHODILATOR agents, *PATIENT satisfaction, *PATIENTS' attitudes
Abstract

A review of the article "Patient Preferences for Symptom-Driven or Regular Preventer Treatment in Mild to Moderate Asthma: Findings From the PRACTICAL Study, a Randomised Clinical Trial," by C. Baggott et al, which appeared in a 2020 issue of the "European Respiratory Journal" is presented.

Published
2020
Full Text
View/download PDF

35. Early-Life Exposure to Oral Antibiotics and Lung Function Into Early Adulthood.

Author

Dagher, Isabelle A. and Kloepfer, Kirsten M.

Subjects
*ANTIBIOTICS, *DRUG resistance in microorganisms, *LUNGS, *MEDICATION errors, *ORAL drug administration, *CHILDREN
Abstract

A review of the article "Early-Life Exposure to Oral Antibiotics and Lung Function Into Early Adulthood," by K. Dos Santos et al, which appeared in a 2020 issue the journal "Chest" is presented.

Published
2020
Full Text
View/download PDF

36. Mediterranean Diet During Pregnancy and Childhood Respiratory and Atopic Outcomes: Birth Cohort Study.

Author

Aguilera, Andrea C. and Kloepfer, Kirsten M.

Subjects
*LUNG physiology, *ECZEMA, *RESPIRATORY diseases, *TREATMENT effectiveness, *POPULATION health, *MEDITERRANEAN diet, *PREGNANCY, *CHILDREN
Abstract

A review of the article "Mediterranean Diet During Pregnancy and Childhood Respiratory and Atopic Outcomes: Birth Cohort Study," by A. Bédard et al, which appeared in a 2020 issue of the periodical "European Respiratory Journal" is presented.

Published
2020
Full Text
View/download PDF

38. Preventing asthma in high risk kids (PARK) with omalizumab: Design, rationale, methods, lessons learned and adaptation.

Author

Phipatanakul, Wanda, Mauger, David T., Guilbert, Theresa W., Bacharier, Leonard B., Durrani, Sandy, Jackson, Daniel J., Martinez, Fernando D., Fitzpatrick, Anne M., Cunningham, Amparito, Kunselman, Susan, Wheatley, Lisa M., Bauer, Cindy, Davis, Carla M., Geng, Bob, Kloepfer, Kirsten M., Lapin, Craig, Liu, Andrew H., Pongracic, Jacqueline A., Teach, Stephen J., and Chmiel, James

Subjects
*OMALIZUMAB, *ASTHMA, *TRANSFORMATIVE learning, *WHEEZE, *RHINITIS, *ANTIBODY formation, *VIRUS diseases, *IMMUNE response
Abstract

Asthma remains one of the most important challenges to pediatric public health in the US. A large majority of children with persistent and chronic asthma demonstrate aeroallergen sensitization, which remains a pivotal risk factor associated with the development of persistent, progressive asthma throughout life. In individuals with a tendency toward Type 2 inflammation, sensitization and exposure to high concentrations of offending allergens is associated with increased risk for development of, and impairment from, asthma. The cascade of biological responses to allergens is primarily mediated through IgE antibodies and their production is further stimulated by IgE responses to antigen exposure. In addition, circulating IgE impairs innate anti-viral immune responses. The latter effect could magnify the effects of another early life exposure associated with increased risk of the development of asthma – viral infections. Omalizumab binds to circulating IgE and thus ablates antigen signaling through IgE-related mechanisms. Further, it has been shown restore IFN-α response to rhinovirus and to reduce asthma exacerbations during the viral season. We therefore hypothesized that early blockade of IgE and IgE mediated responses with omalizumab would prevent the development and reduce the severity of asthma in those at high risk for developing asthma. Herein, we describe a double-blind, placebo-controlled trial of omalizumab in 2–3 year old children at high risk for development of asthma to prevent the development and reduce the severity of asthma. We describe the rationale, methods, and lessons learned in implementing this potentially transformative trial aimed at prevention of asthma. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

39. Phase 3 Trial of Epicutaneous Immunotherapy in Toddlers with Peanut Allergy.

Author

Greenhawt M, Sindher SB, Wang J, O'Sullivan M, du Toit G, Kim EH, Albright D, Anvari S, Arends N, Arkwright PD, Bégin P, Blumchen K, Bourrier T, Brown-Whitehorn T, Cassell H, Chan ES, Ciaccio CE, Deschildre A, Divaret-Chauveau A, Dorris SL, Dorsey MJ, Eiwegger T, Erlewyn-Lajeunesse M, Fleischer DM, Ford LS, Garcia-Lloret M, Giovannini-Chami L, Hourihane JO, Jay N, Jones SM, Kerns LA, Kloepfer KM, Leonard S, Lezmi G, Lieberman JA, Lomas J, Makhija M, Parrish C, Peake J, Perrett KP, Petroni D, Pfützner W, Pongracic JA, Quinn P, Robison RG, Sanders G, Schneider L, Sharma HP, Trujillo J, Turner PJ, Tuttle K, Upton JE, Varshney P, Vickery BP, Vogelberg C, Wainstein B, Wood RA, Bee KJ, Campbell DE, Green TD, Rouissi R, Peillon A, Bahnson HT, Bois T, Sampson HA, and Burks AW

Subjects
Child, Preschool, Humans, Infant, Allergens adverse effects, Arachis adverse effects, Administration, Cutaneous, Anaphylaxis etiology, Desensitization, Immunologic adverse effects, Desensitization, Immunologic methods, Peanut Hypersensitivity complications, Peanut Hypersensitivity therapy
Abstract

Background: No approved treatment for peanut allergy exists for children younger than 4 years of age, and the efficacy and safety of epicutaneous immunotherapy with a peanut patch in toddlers with peanut allergy are unknown., Methods: We conducted this phase 3, multicenter, double-blind, randomized, placebo-controlled trial involving children 1 to 3 years of age with peanut allergy confirmed by a double-blind, placebo-controlled food challenge. Patients who had an eliciting dose (the dose necessary to elicit an allergic reaction) of 300 mg or less of peanut protein were assigned in a 2:1 ratio to receive epicutaneous immunotherapy delivered by means of a peanut patch (intervention group) or to receive placebo administered daily for 12 months. The primary end point was a treatment response as measured by the eliciting dose of peanut protein at 12 months. Safety was assessed according to the occurrence of adverse events during the use of the peanut patch or placebo., Results: Of the 362 patients who underwent randomization, 84.8% completed the trial. The primary efficacy end point result was observed in 67.0% of children in the intervention group as compared with 33.5% of those in the placebo group (risk difference, 33.4 percentage points; 95% confidence interval, 22.4 to 44.5; P<0.001). Adverse events that occurred during the use of the intervention or placebo, irrespective of relatedness, were observed in 100% of the patients in the intervention group and 99.2% in the placebo group. Serious adverse events occurred in 8.6% of the patients in the intervention group and 2.5% of those in the placebo group; anaphylaxis occurred in 7.8% and 3.4%, respectively. Serious treatment-related adverse events occurred in 0.4% of patients in the intervention group and none in the placebo group. Treatment-related anaphylaxis occurred in 1.6% in the intervention group and none in the placebo group., Conclusions: In this trial involving children 1 to 3 years of age with peanut allergy, epicutaneous immunotherapy for 12 months was superior to placebo in desensitizing children to peanuts and increasing the peanut dose that triggered allergic symptoms. (Funded by DBV Technologies; EPITOPE ClinicalTrials.gov number, NCT03211247.)., (Copyright © 2023 Massachusetts Medical Society.)

Published
2023
Full Text
View/download PDF

40. Dysbiotic lung microbial communities of neonates from allergic mothers confer neonate responsiveness to suboptimal allergen.

Author

Bloodworth JC, Hoji A, Wolff G, Mandal RK, Schmidt NW, Deshane JS, Morrow CD, Kloepfer KM, and Cook-Mills JM

Abstract

In humans and animals, offspring of allergic mothers have increased responsiveness to allergens. This is blocked in mice by maternal supplementation with α-tocopherol (αT). Also, adults and children with allergic asthma have airway microbiome dysbiosis with increased Proteobacteria and may have decreased Bacteroidota. It is not known whether αT alters neonate development of lung microbiome dysbiosis or whether neonate lung dysbiosis modifies development of allergy. To address this, the bronchoalveolar lavage was analyzed by 16S rRNA gene analysis (bacterial microbiome) from pups of allergic and non-allergic mothers with a basal diet or αT-supplemented diet. Before and after allergen challenge, pups of allergic mothers had dysbiosis in lung microbial composition with increased Proteobacteria and decreased Bacteroidota and this was blocked by αT supplementation. We determined whether intratracheal transfer of pup lung dysbiotic microbial communities modifies the development of allergy in recipient pups early in life. Interestingly, transfer of dysbiotic lung microbial communities from neonates of allergic mothers to neonates of non-allergic mothers was sufficient to confer responsiveness to allergen in the recipient pups. In contrast, neonates of allergic mothers were not protected from development of allergy by transfer of donor lung microbial communities from either neonates of non-allergic mothers or neonates of αT-supplemented allergic mothers. These data suggest that the dysbiotic lung microbiota is dominant and sufficient for enhanced neonate responsiveness to allergen. Importantly, infants within the INHANCE cohort with an anti-inflammatory profile of tocopherol isoforms had an altered microbiome composition compared to infants with a pro-inflammatory profile of tocopherol isoforms. These data may inform design of future studies for approaches in the prevention or intervention in asthma and allergic disease early in life., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Bloodworth, Hoji, Wolff, Mandal, Schmidt, Deshane, Morrow, Kloepfer and Cook-Mills.)

Published
2023
Full Text
View/download PDF

41. Management of food allergy in the school setting.

Author

Huddleston CM, Kloepfer KM, Jin JJ, and Vitalpur GV

Abstract

Food allergy is a growing health and safety concern that affects up to 8% of school-age children. Because children spend a significant part of their day in school, and the overall number of school-age children with food allergy has been increasing, management of food allergies relies on the collaboration of allergists, families, and schools to treat and prevent acute allergic reactions. For schools, this involves policies centered on food allergen avoidance, preparedness with epinephrine autoinjectors, adequate school personnel training, and accommodations for an equal opportunity learning environment. Partnerships with allergists, primary care providers, students, families, school nurses, and school staff are vital for creating individualized and effective care plans that will allow all children, including those with food allergies, a safe and nurturing learning environment., Competing Interests: The authors have no conflicts of interest to declare pertaining to this article, (Copyright © 2020, The Author(s). Published by OceanSide Publications, Inc., U.S.A.)

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results