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1. Immunity to virus infection (excluding retroviruses) (PP-025)

Author

R. M. Welsh, H. Momtaz, A. R. Thomsen, Y. Watanabe, V. Combes, X. Kong, W. T. Rothwell, M. Kanno, B. Kazemi, A. Shirani, D. Khachapuridze, M. Odenthal, R. Yanagisawa, Z. Ling, P. S. Ohashi, M. L. Freeman, Y. Lee, M Hernández, J. Miles, G. N. Milligan, Z. Liang, Paul G. Thomas, J. Tanaka, Ralph A. Tripp, E. Aguirre, S. Workman, A. Aguilar-Setien, T. Laurinolli, S. Lin, D. Kłosowska, S. Wang, O. Ikeda, K. Ostrow, K. Bogunia-Kubik, U. Kalinke, K. Lee, T. M. Ha, Katherine Kedzierska, G. K. Vikulov, M. Khodabandeh, R. J. Betts, Lisbeth Berrueta, M. Pasparakis, E. Kekäläinen, M. Hoshi, Z. Zeng, T. Toma, G. E. Kaiko, K. Huang, K. S. Lang, T. Ito, R. Hancock, L. Pham Van, U. B. Hellstrom, A. Lange, A. Meyers, R. Petraityte, E. Rizopulu, F. Xu, R. M. Zinkernagel, Y. Girerd-Chambaz, Katayoun Samimi-Rad, Seyed Moayed Alavian, T. Hsu, M. Schaller, D. S. Bowden, M. S. Rolph, H. Fujii, P. A. Lang, M. Akihiro, T. Furuta, S. P. Sylvan, Florian Kern, H. Shibata, Y. Ogawa, X. Zhang, F. Lai, H. Kida, U. Kumaraguru, J. Cardosa, Peter C. Doherty, Mark M. Davis, J. Pätzold, M. Matloubian, Y. Sakoda, P. Chaux, S. Lai, N. Nakajima, Y. Chen, K. Markiewicz, T. Tran, P. Chong, I. Lagereva, B. Sierra, E. Nazarov, M. Kikuchi, H. Ishida, C. Ferrari, David L. Woodland, A. G. Bean, M. H. Nelson, Z. J. Chen, D. M. Estes, M. R. Azar Pajoh, K. Vogt, M. A. Blackman, R. Todaka, S. Ma, W. Li, J. Sun, P. Lukianov, K. Gärtner, A. Vaheri, P. Wark, A. W. S. Yeung, A. Matsumura, L. Cao, I. Beĭkin, M. Recher, K. Eriksson, V. Wang, D. Webster, H. Yoshizawa, K. Hosiawa-Meagher, P. Sun, K. Katayama, H. Bisceglia, J. Du, M. Matsumoto, Z. Qu, P. J. Gaddi, M. R. Edwards, J. R. Carlyle, T. U. Aripova, A. G. Telcian, J. S. Yi, V. I. Afanasyeva, R. Kumar, B. Shaffaedin, S. Schoenberger, A. S. Khodjaeva, S. C. Weaver, D. Verthelyi, R. Sugamata, F. Ershov, R. Jafari Shakib, G. N. Feketea, A. Brook, H. Lei, Z. Qin, F. Vahedi, M. G. Guzmán, J. Huang, C. Ventura, A. Izquierdo, W. Siew Cheng, T. Kawamura, H. Keyvani, C. Ørskov, C. Tami, T. T. Tran, J. H. Fine, H. Kato, Z. J. Rakhmankulova, Y. A. Chen, J. C. Huang, K. Kobayashi, K. Kitamura, W. F. Carson, Azam Bolhassani, R. Rochford, J. Li, M. A. Bolkov, H. Liu, T. Ospelnikova, P. Storm, S. T. Smiley, L. A. Stanciu, F. Sánchez-García, M. Nakayama, M. B. Moreno-Altamrano, T. Wada, J. Deng, A. Perez, M. Puig, N. W. Lukacs, G. Liang, S. Jeon, L. C. Bonifaz-Alfonzo, S. Shimada, G. García, H. Marshall, A. Górski, S. Phipps, H. Tran, H. Kanegane, G. Korczak-Kowalska, C. Boni, J. Kyd, L. Rocha-Zavaleta, F. Garib, H. T. Q. Vu, M. Simadu, J. P. Twohig, B. G. Oliver, Shine Thomas, D. Chu, S. M. Cuff, Y. Lin, Z. Tian, S. Mäkelä, N. Mosaffa, M. Gołebiowska Wawrzyniak, R. Anderson, M. Brückel, T. P. Salazar-Mather, G. E. Grau, H. G. Durkin, I. R. Humphreys, W. Xi, H. Lin, Y. Sakakibara, A. Toga, P. Chen, K. Saito, Yasaman Taslimi, Leidith Berrueta-Carrillo, Y. Itoh, J. Sung, F. Liao, V. Emery, Y. Sato, S. Voigt, H. Horie, L. Simson, M. Larki, A. Hayashi, S. L. Rossi, R. Milne, R. Mirzaei, B. Evengård, Y. Liu, P. G. Mohr, B. Weiss-Steider, T. Nishimura, M. J. Crane, M. Høgh-Petersen, E. Sandalova, A. Dehghan, Z. Sharifnia, E. C. Y. Wang, H. Volk, M. L. Mora-García, C. M. Hogaboam, J. M. Clingan, A. T. Tan, N. Evstigneeva, P. Knolle, S. Hsieh, I. Kucinskaite-Kodze, M. Alvarez, Darrell L. Peterson, D. Tran, Sima Rafati, T. Seya, S. Marques, Tania Cukalac, F. Goshima, L. Perea-Martìnez, N. La Gruta, S. Kawachi, I. Hirono, M. Raeiszadeh, M. Koura, P. Holst, P. Kourilsky, R. Ganjali, J. P. Christensen, N. Hirankarn, L. Yao, A. Jakimiuk, J. Browne, I. V. Nesterova, M. Lu, M. Rezvani, C. Lin, B. A. Wu-Hsieh, G. P. Nolan, L. P. Bykova, B. Agrawal, K. Pérz-Saldaña, P. M. Niedzwiedzka-Rystwej, B. Pliego-Rivero, M. Farhadi, A. P. Godovalov, E. W. Newell, G. Hsu, L. T. P. Nguyen, Y. Chang, F. Rashidi, J. Tanguy, P. Kaiser, H. Lauterbach, F. Saito, R. Chua, P. W. Mason, I. A. Pashnina, H. Neekdan, Jamie Rossjohn, M. Toporkova, Luisa Barboza, H. Mitsui, M. C. Zaragoza-Ortega, E. L. Istomina, L. T. Dang, S. N. Boyarsky, A. Mesci, S. Vázquez, O. A. Aguilar, K. Shinoda, C. G. Silva, Stacie Woolard, M. Sadeghi, M. Jones, Farnaz Zahedifard, L. Wyatt, H. Dobashi, J. Simas, Henry Montes, N. Levchik, P. Kokhaei, C. Bartholdy, S. L. Kunkel, K. Suzuki, E. E. Ooi, Ashish Kumar, I. P. Balmasova, J. Ettinger, T. Nakayama, A. J. Zajac, R. Eftekhari, R. Lachmann, H. Inoue, D. Häussinger, D. Zhao, S. Koyasu, Chi Ma, Y. Keynan, M. V. Chikhladze, A. Hsu, F. Khodapanahandeh, W. Sun, K. Ogasawara, L. S. Tsai, M. Asano, A. Yachie, Stephanie Gras, J. Körner, N. Gaius, R. Gholamian-Dehkordi, Y. R. Sepiashvili, Y. Lu, Xinghao Ding, N. Vasilakis, D. Laccabue, H. Wu, J. Feng, S. Liu, X. Liang, M. Nowakowski, M. Krönke, K. I. Mattaei, D. V. Tran, K. L. O. Antonsdotter, K. Wong, B. Tzang, B. Dabirmanesh, H. Hochrein, Stephen J. Turner, A. Kulawik, D. Omagari, L. Skljar, O. Kovalenko, M. Seishima, H. Dienes, E. Rubinstein, L. Cervantes-Barragan, Y. Kim, I. Moro, U. Protzer, R. Sun, T. Mironova, D. M. Kemeny, J. Tavakkol Afshari, J. Mustonen, J. W. Lowenthal, T. P. Arstila, S. Kiabi, J. L. Munoz-Jordan, Z. S. Kamalov, Z. Wawrzyniak, C. Ahlm, K. Soda, Z. Mohtasham Amiri, Y. Aratani, T. Chumachenko, Y. Teruhito, Ali Eslamifar, J. Pedras-Vasconcelos, A. P. Durbin, N. J. C. King, H. Vu, M. Suter, T. Burgess, Z. Atai, T. Vo, E. R. Jellison, F. Li, M. C. Mohanty, E. V. Vlasova, T. Ball, H. Ishigaki, I. A. Tuzankina, C. R. Stewart, A. Flavigny, L. Nguyen, T. Sata, S. Akira, V. Kalihevich, E. Jaskula, O. Takeuchi, C. Aitken, K. Mohtashami, M. Bharadwaj, A. Bertoletti, Melisa Colmenares, H. Jenssen, S. Chen, J. Ramos-Castaneda, J. S. Ahn, D. Xilei, L. Hsu, A. Verschoor, M. Bandehpour, H. D. Volk, M. H. Bluth, M. Du, M. Tadashi, S. Mahalingam, C. Tsai, M. Arikata, Sophie A. Valkenburg, A. Monroy-García, M. Okamatsu, K. Rytwinski, K. Schmolke, D. B. Lewis, Siham Salmen, H. A. Mahgoub, C. Butts, A. Krishnamurthy, S. Moneer, H. Kondo, Ali Khamesipour, P. Ghyasemi-Dehkordi, L. Valdés, R. Aoki, L. A. Sandoval-Escobar, H. Ito, Natasha G. Swan, K. Dahlman-Wright, B. J. Hanson, P. M. Hansbro, P. Foster, M. Yasunami, Q. Ge, K. Tomizawa, U. Nivarthi, W. Wu, J. McCluskey, Y. Wang, J. Lee, J. McGrath, K. Yamamoto, J. Jan, L. Kjer-Nielsen, S. L. Johnston, H. Takaki, N. Prabhu, T. J. Standiford, B. Moss, L. Sanchez, P. Sodsai, M. Guzman, P. S. Foster, E. V. Shmeleva, A. Shestakov, T. Satoh, R. S. Kuzyaev, P. Wierzbicki, K. Fink, H. Rafat Panah, H. Ohtaki, J. Nakkuntod, E. S. Malova, K. Hirayama, H. Yagita, A. Zvirbliene, S. V. Mayer, B. Jin, L. Zuo, Z. Ardemasova, N. Harris, A. Kozar, S. Vostrukhin, J. Chang, C. Zhao, S. Kurata, S. Noorbakhsh, M. Muramatsu, E. Guillemard, O. Mikhailova, T. V. Vo, C. Fuentes-Miranda, P. Chaplin, D. Stabenow, N. Burdin, S. C. D. D. Abedelmalek, Y. Kuznetsova, Mohammad Taghikhani, D. K. Hong, A. B. Pérez, S. Yuichi, J. Hernández-Montes, O. Cruz y Cruz, T. Maciejewski, G. Siritsa, Elham Mohit, K. Morita, Y. Jiang, D. K. Krishnadas, K. Sasnauskas, W. M. Deptuła, H. Nguyen, J. Borysowski, K. Komiyama, C. Chuang, E. Markelova, N. Babel, K. R. Fowke, D. Thammanichanond, R. Kassub, C. Chirathaworn, A. Rizopulu, I. Gorelova, N. Van Rooijen, F. Pak, N. Bourne, D. Townsend, C. Krings, Y. Nishiyama, B. Ludewig, E. R. Winkelmann, J. M. Deshpande, S. Tsai, P. A. MacAry, Y. Mitsuya, S. Marashi, J. Niu, N. Watanabe, J. Schrezenmeir, R. M. Locksley, J. Jang, N. D. Yushchuk, Y. Su, S. Chowdhury, J. A. Juno, F. Ghazi, M. Hellard, H. Hengartner, Y. Ohmoto, W. Yang, R. B. Tesh, A. W. Ho, P. Kupatawintu, Z. Wang, P. Brundin, S. de la Motte, S. C. Bendall, M. Oshima, P. Tangkijvanich, T. Nagao, and B. M. M. Moreno-Altamirano

Subjects
Immunity, Immunology, Immunology and Allergy, General Medicine, Biology, Virology, Virus, Oncovirus
Published
2010
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2. Alveolar macrophages are required for protective pulmonary defenses in murine Klebsiella pneumonia: elimination of alveolar macrophages increases neutrophil recruitment but decreases bacterial clearance and survival

Author

S L Kunkel, T J Standiford, E Broug-Holub, G B Toews, R M Strieter, J F van Iwaarden, R. rd. Paine, and VU University medical center

Subjects
Neutrophils, Immunology, Inflammation, Biology, Microbiology, Mice, In vivo, Macrophages, Alveolar, Pneumonia, Bacterial, medicine, Animals, Lung, Immunity, Cellular, Respiratory disease, Bacterial pneumonia, medicine.disease, Klebsiella Infections, Klebsiella pneumoniae, Infectious Diseases, medicine.anatomical_structure, Parasitology, Tumor necrosis factor alpha, Klebsiella pneumonia, medicine.symptom, Pulmonary alveolus, Research Article
Abstract

To study the in vivo role of alveolar macrophages (AM) in gram-negative bacterial pneumonia in mice, AM were eliminated by the intratracheal (i.t.) administration of dichloromethylene diphosphonate encapsulated liposomes. Subsequently, the AM-depleted mice were infected i.t. with 100 CFU of Klebsiella pneumoniae, and the effects of AM depletion on survival, bacterial clearance, and neutrophil (polymorphonuclear leukocyte [PMN]) recruitment were assessed. It was shown that depletion of AM decreases survival dramatically, with 100% lethality at day 3 postinfection, versus 100% long-term survival in the control group. This increased mortality was accompanied by 20- to 27- and 3- to 10-fold increases in the number of K. pneumoniae CFU in lung and plasma, respectively, compared to those in nondepleted animals. This decreased bacterial clearance was not due to an impaired PMN recruitment; on the contrary, the K. pneumoniae-induced PMN recruitment in AM-depleted lungs was sevenfold greater 48 h postinfection than that in control infected lungs. Together with an increased PMN infiltration, 3- and 10-fold increases in lung homogenate tumor necrosis factor alpha (TNF-alpha) and macrophage inflammatory protein 2 (MIP-2) levels, respectively, were measured. Neutralization of TNF-alpha or MIP-2, 2 h before infection, reduced the numbers of infiltrating PMN by 41.6 and 64.2%, respectively, indicating that these cytokines mediate PMN influx in infected lungs, rather then just being produced by the recruited PMN themselves. Our studies demonstrate, for the first time, the relative importance of the AM in the containment and clearance of bacteria in the setting of Klebsiella pneumonia.

Published
1997
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3. Interleukin-8 production in red blood cell incompatibility

Author

R D, Davenport, R M, Strieter, T J, Standiford, and S L, Kunkel

Subjects
Erythrocytes, Time Factors, Base Sequence, Dose-Response Relationship, Drug, Interleukin-8, Molecular Sequence Data, Immunology, Gene Expression, Transfusion Reaction, Cell Biology, Hematology, Blotting, Northern, Hemolysis, Biochemistry, ABO Blood-Group System, Blood Group Incompatibility, Humans, RNA, Oligonucleotide Probes
Abstract

Hemolytic transfusion reactions (HTR) are characterized by fever, shock, organ system failure, intravascular coagulation, and possibly death. The same findings may be associated with sepsis. Neutrophils have been implicated in the pathogenesis of HTR, although a mechanism for neutrophil activation has not been shown. In addition, the possible role that cytokines may play in HTR has not been investigated. We show that interleukin-8 (IL-8), a cytokine with chemotactic and neutrophil- activation properties, is produced in whole blood following addition of ABO-incompatible red blood cells, in a dose- and time-dependent manner related to the degree of hemolysis, and is inhibited by inactivation of complement. IL-8 production is accompanied by increased gene expression in the buffy coat. This observation has implications for the understanding of the pathogenesis of and for the treatment of HTR.

Published
1990
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4. The production of interleukin-1 receptor antagonist by human bronchogenic carcinoma

Author

D R, Smith, S L, Kunkel, T J, Standiford, S W, Chensue, M W, Rolfe, M B, Orringer, R I, Whyte, M D, Burdick, J M, Danforth, and A R, Gilbert

Subjects
Interleukin 1 Receptor Antagonist Protein, Carcinoma, Bronchogenic, Lung Neoplasms, Sialoglycoproteins, Blotting, Western, Carcinoma, Squamous Cell, Tumor Cells, Cultured, Humans, Enzyme-Linked Immunosorbent Assay, Adenocarcinoma, Immunohistochemistry, Regular Articles
Abstract

Bronchogenic carcinoma displays an aggressive clinical course that may reflect a capacity to evade host defenses. We postulated that tumors may elaborate interleukin-1 receptor antagonist protein (IRAP) to escape host interleukin-1-dependent responses. Homogenates of human bronchogenic lung tumors demonstrated significant increases of IRAP compared with normal lung tissue controls (n = 48). There was no significant difference in interleukin-1 beta levels between tumor and normal lung tissue. Immunohistochemical staining localized IRAP to tumor cells. Semiquantitative pathological analysis demonstrated a modest inflammatory cell infiltrate with qualitative differences between tumors of different histology. Western blot analysis of tumor homogenates demonstrated several molecular weight forms of IRAP. Finally, antigenic IRAP was detected in supernatants of the human bronchogenic carcinoma cell line (A549) maintained in vitro. These findings illustrate the capacity of bronchogenic tumors to produce and secrete IRAP that may be important in tumor evasion of host defenses.

Published
1993

5. Cytokine-induced neutrophil-derived interleukin-8

Author

R M, Strieter, K, Kasahara, R M, Allen, T J, Standiford, M W, Rolfe, F S, Becker, S W, Chensue, and S L, Kunkel

Subjects
Lipopolysaccharides, Time Factors, Dose-Response Relationship, Drug, Neutrophils, Tumor Necrosis Factor-alpha, Interleukin-8, Drug Synergism, Immunohistochemistry, Cell Adhesion, Cytokines, Humans, RNA, Messenger, Antigens, Plastics, Interleukin-1, Research Article
Abstract

During acute inflammation, the first line of cellular response for host defense is the neutrophil. In addition to the historic role of the neutrophil as a phagocyte, recent studies have identified this cell as an important source of a number of cytokines. In this study, we provide evidence that the neutrophil is a significant source of interleukin-8 (IL-8). Neutrophils freshly isolated from whole blood were not found to constitutively express IL-8 mRNA. In contrast, when these leukocytes were cultured on plastic they were activated, leading to the significant expression of de novo steady-state levels of IL-8 mRNA. In addition, when neutrophils were treated with cycloheximide, there was evidence for "superinduction" of steady-state levels of IL-8 mRNA and inhibition of antigenic IL-8 production. Neutrophils were subsequently stimulated with lipopolysaccharide (LPS), tumor necrosis factor-alpha, or interleukin-1-beta and were found to express IL-8 mRNA and antigen in both a time- and dose-dependent manner. Furthermore, neutrophils stimulated with traditional chemotactic/activating factors, such as the split product of the fifth component of complement (C5a), formylmethionyleucylphenylalanine (fMLP), and leukotriene B4 (LTB4) in a dose-dependent manner did not produce significant antigenic IL-8, as compared with unstimulated controls. In contrast, when neutrophils were exposed to either of these neutrophil agonists in the presence of LPS, the production of antigenic IL-8 was significantly elevated, as compared with either of the stimuli alone, suggesting a synergistic response. These data would suggest that the neutrophil can no longer be viewed as only a phagocyte or warehouse for proteolytic enzymes, but is a pivotal effector cell that is able to respond to mediators in its environment and generate cytokines. This latter neutrophil response may be important for either the elicitation of additional neutrophils or to orchestrate the conventional immune response at sites of inflammation.

Published
1992

6. Alveolar macrophage-derived cytokines induce monocyte chemoattractant protein-1 expression from human pulmonary type II-like epithelial cells

Author

T J, Standiford, S L, Kunkel, S H, Phan, B J, Rollins, and R M, Strieter

Subjects
Chemotactic Factors, Tumor Necrosis Factor-alpha, Macrophages, Epithelial Cells, Blotting, Northern, Pulmonary Alveoli, Gene Expression Regulation, Cytokines, Humans, RNA, Messenger, Lung, Chemokine CCL2, Chromatography, High Pressure Liquid, Interleukin-1
Abstract

Many acute and chronic lung diseases are characterized by the presence of increased numbers of activated macrophages. These macrophages are derived predominantly from newly recruited peripheral blood monocytes and may play a role in the amplification and perpetuation of an initial lung insult. The process of inflammatory cell recruitment is poorly understood, although the expression of inflammatory cell-specific chemoattractants and subsequent generation of chemotactic gradients is likely involved. Although immune cells such as macrophages and lymphocytes are known to generate several inflammatory cell chemoattractants, parenchymal cells can also synthesize and secrete a number of bioactive factors. We now demonstrate the generation of significant monocyte chemotactic activity from tumor necrosis factor (TNF)-alpha and interleukin (IL)-1 beta-treated pulmonary type II-like epithelial cells (A549). The predominant inducible monocyte chemotaxin had an estimated molecular mass of approximately 14-15 kDa and was neutralized by specific antibody to human monocyte chemotactic protein-1 (MCP-1). Induction of activity was accompanied by increases in steady-state mRNA level for MCP-1. These data are consistent with the induction of MCP-1 expression from A549 cells by TNF and IL-1. MCP-1 production from A549 cells could be induced by lipopolysaccharide (LPS)-stimulated alveolar macrophage (AM)-conditioned media, but not by LPS alone. The inducing activity in AM-conditioned media was neutralized with specific antibodies to IL-1 beta, but not TNF-alpha. Our findings suggest that the alveolar epithelium can participate in inflammatory cell recruitment via the production of MCP-1 and that cytokine networking between contiguous alveolar macrophages and the pulmonary epithelium may be essential for parenchymal cell MCP-1 expression.

Published
1991

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