Innate resistance and responses to HIV

2012 ◽  
Author(s):  
Jason Brenchley
Keyword(s):  
Innate Resistance

Microbial exposure early in life regulates airway inflammation in mice after infection with Streptococcus pneumoniae with enhancement of local resistance

2010 ◽  
Vol 298 (1) ◽  
pp. L67-L78 ◽  
Author(s):  
Yasuki Yasuda ◽  
Yoko Matsumura ◽  
Kazuki Kasahara ◽  
Noriko Ouji ◽  
Shigeki Sugiura ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Pneumococcal Infection ◽  
Hygiene Hypothesis ◽  
Respiratory Pathogen ◽  
T Helper 1 ◽  
Innate Resistance ◽  
Anaerobic Microorganisms ◽  
Early Life Exposure ◽  
Microbial Extracts ◽  
Microbial Exposure

The immunological explanation for the “hygiene hypothesis” has been proposed to be induction of T helper 1 (Th1) responses by microbial products. However, the protective results of hygiene hypothesis-linked microbial exposures are currently shown to be unlikely to result from a Th1-skewed response. Until now, effect of microbial exposure early in life on airway innate resistance remained unclear. We examined the role of early life exposure to microbes in airway innate resistance to a respiratory pathogen. Specific pathogen-free weanling mice were nasally exposed to the mixture of microbial extracts or PBS (control) every other day for 28 days and intratracheally infected with Streptococcus pneumoniae 10 days after the last exposure. Exposure to microbial extracts facilitated colonization of aerobic gram-positive bacteria, anaerobic microorganisms, and Lactobacillus in the airway, compared with control exposure. In pneumococcal pneumonia, the exposure prolonged mouse survival days by suppressing bacterial growth and by retarding pneumococcal blood invasion, despite significantly low levels of leukocyte recruitment in the lung. Enhancement of airway resistance was associated with a significant decrease in production of leukocyte chemokine (KC) and TNFα, and suppression of matrix metalloproteinase (MMP-9) expression/activation with enhancement of tissue inhibitor of MMP (TIMP-3) activation. The exposure increased production of IFN-γ, IL-4, and monocyte chemoattractant-1 following infection. Furthermore, expression of Toll-like receptor 2, 4, and 9 was promoted by the exposure but no longer upregulated upon pneumococcal infection. Thus, we suggest that hygiene hypothesis is more important in regulating the PMN-dominant inflammatory response than in inducing a Th1-dominant response.

scholarly journals The innate resistance of Trypanosoma copemani to human serum

2015 ◽  
Vol 153 ◽  
pp. 105-110 ◽  
Author(s):  
J.M. Austen ◽  
U. Ryan ◽  
W.G.F. Ditcham ◽  
J.A. Friend ◽  
S.A. Reid
Keyword(s):  
Human Serum ◽  
Innate Resistance
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