دورية أكاديمية

Dysregulation of TNF-α and IFN-γ expression is a common host immune response in a chronically infected mouse model of melioidosis when comparing multiple human strains of Burkholderia pseudomallei.

التفاصيل البيبلوغرافية
العنوان: Dysregulation of TNF-α and IFN-γ expression is a common host immune response in a chronically infected mouse model of melioidosis when comparing multiple human strains of Burkholderia pseudomallei.
المؤلفون: Amemiya K; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA. kei.amemiya.vol@mail.mil., Dankmeyer JL; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Bearss JJ; Pathology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Zeng X; Pathology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Stonier SW; Virology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Soffler C; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Cote CK; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Welkos SL; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Fetterer DP; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Chance TB; Pathology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Trevino SR; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Worsham PL; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA., Waag DM; Bacteriology Division, US Army Medical Research Institute of Infectious Diseases, Fort Detrick, Frederick, MD, USA.
المصدر: BMC immunology [BMC Immunol] 2020 Feb 03; Vol. 21 (1), pp. 5. Date of Electronic Publication: 2020 Feb 03.
نوع المنشور: Comparative Study; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
اللغة: English
بيانات الدورية: Publisher: BioMed Central Country of Publication: England NLM ID: 100966980 Publication Model: Electronic Cited Medium: Internet ISSN: 1471-2172 (Electronic) Linking ISSN: 14712172 NLM ISO Abbreviation: BMC Immunol Subsets: MEDLINE
أسماء مطبوعة: Original Publication: London : BioMed Central, [2000-
مواضيع طبية MeSH: Burkholderia pseudomallei/*physiology , Interferon-gamma/*metabolism , Melioidosis/*immunology , Spleen/*pathology , Tumor Necrosis Factor-alpha/*metabolism, Animals ; Chronic Disease ; Disease Models, Animal ; Humans ; Immunity, Cellular ; Mice ; Mice, Inbred BALB C
مستخلص: Background: Melioidosis is endemic in Southeast Asia and Northern Australia and is caused by the Gram-negative, facultative intracellular pathogen Burkholderia pseudomallei. Diagnosis of melioidosis is often difficult because of the protean clinical presentation of the disease, and it may mimic other diseases, such as tuberculosis. There are many different strains of B. pseudomallei that have been isolated from patients with melioidosis, but it was not clear if they could cause a similar disease in a chronic BALB/c murine model of melioidosis. Hence, we wanted to examine chronically infected mice exposed to different strains of B. pseudomallei to determine if there were differences in the host immune response to the pathogen.
Results: We identified common host immune responses exhibited in chronically infected BALB/c mice, although there was some heterogeneity in the host response in chronically infected mice after exposure to different strains of B. pseudomallei. They all displayed pyogranulomatous lesions in their spleens with a large influx of monocytes/macrophages, NK cells, and neutrophils identified by flow cytometry. Sera from chronically infected mice by ELISA exhibited elevated IgG titers to the pathogen, and we detected by Luminex micro-bead array technology a significant increase in the expression of inflammatory cytokines/chemokines, such as IFN-γ, IL-1α, IL-1β, KC, and MIG. By immunohistochemical and in situ RNA hybridization analysis we found that the increased expression of proinflammatory cytokines (IL-1α, IL-1β, TNF-α, IFN-γ) was confined primarily to the area with the pathogen within pyogranulomatous lesions. We also found that cultured splenocytes from chronically infected mice could express IFN-γ, TNF-α, and MIP-1α ex vivo without the need for additional exogenous stimulation. In addition by flow cytometry, we detected significant amounts of intracellular expression of TNF-α and IFN-γ without a protein transport blocker in monocytes/macrophages, NK cells, and neutrophils but not in CD4 + or CD8 + T cells in splenocytes from chronically infected mice.
Conclusion: Taken together the common features we have identified in chronically infected mice when 10 different human clinical strains of B. pseudomallei were examined could serve as biomarkers when evaluating potential therapeutic agents in mice for the treatment of chronic melioidosis in humans.
References: J Immunol. 2012 Sep 1;189(5):2530-6. (PMID: 22837486)
PLoS One. 2018 Nov 30;13(11):e0208277. (PMID: 30500862)
Cell Death Dis. 2015 Jun 18;6:e1792. (PMID: 26086965)
J Immunol. 2015 May 1;194(9):4413-21. (PMID: 25801435)
PLoS One. 2012;7(2):e30789. (PMID: 22363490)
Infect Immun. 2015 Dec;83(12):4759-71. (PMID: 26416901)
Clin Infect Dis. 1999 Aug;29(2):408-13. (PMID: 10476750)
PLoS Negl Trop Dis. 2010 Nov 30;4(11):e900. (PMID: 21152057)
Front Cell Infect Microbiol. 2015 Nov 18;5:80. (PMID: 26636042)
Plant Physiol. 2002 Nov;130(3):1102-8. (PMID: 12427977)
J Antimicrob Chemother. 2004 Dec;54(6):1134-8. (PMID: 15509614)
J Immunol Methods. 2000 Apr 21;238(1-2):107-17. (PMID: 10758241)
J Med Microbiol. 1990 Feb;31(2):109-14. (PMID: 2304065)
PLoS One. 2009 Oct 06;4(10):e7308. (PMID: 19806192)
Trans R Soc Trop Med Hyg. 2004 Nov;98(11):678-86. (PMID: 15363648)
Sci Rep. 2014 Mar 07;4:4305. (PMID: 24603493)
Semin Immunopathol. 2016 Mar;38(2):221-37. (PMID: 26542392)
BMC Infect Dis. 2010 Oct 21;10:302. (PMID: 20964837)
Infect Immun. 2009 Apr;77(4):1589-95. (PMID: 19179418)
Cell Microbiol. 2005 Oct;7(10):1447-58. (PMID: 16153244)
Discov Med. 2013 Sep;16(87):123-31. (PMID: 23998448)
Front Microbiol. 2011 Aug 22;2:170. (PMID: 22007185)
Am J Pathol. 2011 Jul;179(1):270-80. (PMID: 21703409)
Immunol Rev. 2018 Jan;281(1):8-27. (PMID: 29247995)
mBio. 2013 Jul 16;4(4):null. (PMID: 23860767)
J Immunol. 2015 Oct 1;195(7):3248-3261. (PMID: 26311902)
Nat Immunol. 2010 May;11(5):373-84. (PMID: 20404851)
Future Microbiol. 2012 Dec;7(12):1389-99. (PMID: 23231488)
J Infect Dis. 2002 Jul 15;186(2):286-9. (PMID: 12134268)
J Infect Dis. 1992 Mar;165(3):561-4. (PMID: 1538161)
J Clin Microbiol. 2014 Sep;52(9):3418-21. (PMID: 24966357)
PLoS Negl Trop Dis. 2015 Oct 23;9(10):e0004152. (PMID: 26495852)
J Infect Dis. 2007 Jan 1;195(1):99-107. (PMID: 17152013)
Nat Rev Microbiol. 2009 Feb;7(2):99-109. (PMID: 19148178)
Antimicrob Agents Chemother. 2011 Nov;55(11):5388-91. (PMID: 21876049)
Clin Immunol. 2004 Oct;113(1):22-8. (PMID: 15380526)
Infect Immun. 2002 May;70(5):2319-25. (PMID: 11953366)
J Clin Microbiol. 1999 Jan;37(1):225-8. (PMID: 9854098)
Trop Med Int Health. 2004 Nov;9(11):1167-74. (PMID: 15548312)
Int J Antimicrob Agents. 2014 Apr;43(4):310-8. (PMID: 24613038)
J Infect Dis. 2006 Feb 1;193(3):370-9. (PMID: 16388484)
Nat Immunol. 2012 Mar 19;13(4):325-32. (PMID: 22430785)
Front Immunol. 2014 Feb 24;5:70. (PMID: 24605113)
Immunity. 2012 Mar 23;36(3):388-400. (PMID: 22444631)
Am J Trop Med Hyg. 2013 Nov;89(5):983-985. (PMID: 24062474)
N Engl J Med. 2012 Sep 13;367(11):1035-44. (PMID: 22970946)
Nat Rev Immunol. 2014 Feb;14(2):81-93. (PMID: 24445666)
PLoS One. 2017 Feb 24;12(2):e0172627. (PMID: 28235018)
Cytokine Growth Factor Rev. 2009 Apr;20(2):97-113. (PMID: 19268625)
J Immunol. 2005 May 15;174(10):5936-40. (PMID: 15879085)
PLoS Negl Trop Dis. 2009;3(4):e407. (PMID: 19352426)
PLoS Negl Trop Dis. 2016 Mar 14;10(3):e0004503. (PMID: 26974441)
J Lipid Res. 2007 Apr;48(4):751-62. (PMID: 17202130)
Clin Microbiol Rev. 2005 Apr;18(2):383-416. (PMID: 15831829)
Nat Rev Immunol. 2015 Aug;15(8):486-99. (PMID: 26205583)
J Immunol. 2000 Nov 15;165(10):5387-91. (PMID: 11067887)
PLoS Pathog. 2006 Feb;2(2):e4. (PMID: 16518473)
Vaccine. 2006 Feb 27;24(9):1413-20. (PMID: 16213631)
Int J Exp Pathol. 2009 Feb;90(1):16-25. (PMID: 19200247)
Cell Rep. 2015 Jun 16;11(10):1535-48. (PMID: 26027935)
Front Microbiol. 2011 Jan 26;2:2. (PMID: 21687401)
Nat Microbiol. 2016 Jan 11;1:15008. (PMID: 27571754)
PLoS Pathog. 2014 Mar 13;10(3):e1003986. (PMID: 24626296)
Arch Pathol. 1970 Aug;90(2):101-11. (PMID: 5433595)
Infect Immun. 1996 Mar;64(3):782-90. (PMID: 8641782)
Ther Adv Respir Dis. 2011 Aug;5(4):255-73. (PMID: 21372121)
J Mol Diagn. 2012 Jan;14(1):22-9. (PMID: 22166544)
FEMS Immunol Med Microbiol. 2008 Apr;52(3):379-88. (PMID: 18294191)
Clin Diagn Lab Immunol. 2000 Nov;7(6):920-4. (PMID: 11063499)
Semin Immunol. 2014 Dec;26(6):552-8. (PMID: 25444549)
Ann Gastroenterol. 2013;26(1):77-79. (PMID: 24714690)
PLoS Pathog. 2011 Dec;7(12):e1002452. (PMID: 22241982)
Infect Immun. 1999 Jul;67(7):3593-600. (PMID: 10377144)
J Infect Dis. 2007 Sep 1;196(5):782-7. (PMID: 17674322)
Infect Immun. 2000 Apr;68(4):2034-42. (PMID: 10722599)
Microb Pathog. 2015 Sep;86:53-63. (PMID: 26162294)
فهرسة مساهمة: Keywords: BALB/c mice; Burkholderia pseudomallei; Chronic infection; Inflammatory cytokines; Intracellular TNFα and IFNγ; Pyogranulomatous lesion
المشرفين على المادة: 0 (Tumor Necrosis Factor-alpha)
82115-62-6 (Interferon-gamma)
تواريخ الأحداث: Date Created: 20200205 Date Completed: 20201207 Latest Revision: 20201214
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC6998218
DOI: 10.1186/s12865-020-0333-9
PMID: 32013893
قاعدة البيانات: MEDLINE
الوصف
تدمد:1471-2172
DOI:10.1186/s12865-020-0333-9