Stress-induced differences in primary and secondary resistance against bacterial sepsis corresponds with diverse corticotropin releasing hormone receptor expression by pulmonary CD11c+ MHC II+ and CD11c− MHC II+ APCs
Autor: | Khaisha Johnson, Xavier F. Gonzales, Mark Pulse, Aniket Deshmukh, Harlan P. Jones |
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Rok vydání: | 2008 |
Předmět: |
Restraint
Physical Secondary infection Immunology Antigen presentation Antigen-Presenting Cells Corticotropin-releasing hormone receptor Mice Inbred Strains Biology Receptors Corticotropin-Releasing Hormone Pneumococcal Infections Article Mice Behavioral Neuroscience Corticotropin-releasing hormone Immune system Stress Physiological Immunity Sepsis Leukocytes Pneumonia Bacterial medicine Animals Antigen-presenting cell Lung Antigen Presentation Endocrine and Autonomic Systems Histocompatibility Antigens Class II CD11c Antigen Specific Pathogen-Free Organisms medicine.anatomical_structure Female Bronchoalveolar Lavage Fluid Respiratory tract |
Zdroj: | Brain, Behavior, and Immunity. 22:552-564 |
ISSN: | 0889-1591 |
DOI: | 10.1016/j.bbi.2007.11.005 |
Popis: | Stress responses have been associated with altered immunity and depending upon the type of stressor, can have diverse effects on disease outcomes. As the first line of defense against potential pathogens, alterations in cellular immune responses along the respiratory tract can have a significant impact on the manifestation of local and systemic disease. Utilizing a murine model of respiratory pneumonia, the current study investigated the effects of restraint stress on the induction of primary and secondary immunity along the respiratory tract, influencing host susceptibility. Female CD-1 mice were subjected to three hours of restraint stress over a period of four days followed by primary and secondary Streptococcus pneumoniae infection via intranasal route. Stress exposure led to increased retention of bacterial carriage in the lungs, enhanced polymorphonuclear cells and a preferential decrease in pulmonary CD11c(+) MHC II(+) cells resulting in delayed lethality during primary infection but significant impairment of acquired immune protection after secondary infection. We also provide evidence to support a role for lung-associated corticotropin releasing hormone regulation through peripheral CRH and diverse CRH receptor expression by MHC II(+) antigen presenting cells (APCs). We conclude that repeated restraint stress has distinct influences on immune cell populations that appear to be important in the generation of innate and adaptive immune responses along the respiratory tract with the potential to influence local and systemic protection against disease pathogenesis. |
Databáze: | OpenAIRE |
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