A fresh look at the hygiene hypothesis: How intestinal microbial exposure drives immune effector responses in atopic disease

2013 ◽  
Vol 25 (5) ◽  
pp. 378-387 ◽  
Author(s):  
Eric M. Brown ◽  
Marie-Claire Arrieta ◽  
B. Brett Finlay
2010 ◽  
Vol 298 (1) ◽  
pp. L67-L78 ◽  
Author(s):  
Yasuki Yasuda ◽  
Yoko Matsumura ◽  
Kazuki Kasahara ◽  
Noriko Ouji ◽  
Shigeki Sugiura ◽  
...  

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.


2002 ◽  
Vol 14 (6) ◽  
pp. 676-677 ◽  
Author(s):  
Ramsay L. Fuleihan

2004 ◽  
Vol 38 (4) ◽  
pp. 378-388 ◽  
Author(s):  
Samuli Rautava ◽  
Olli Ruuskanen ◽  
Arthur Ouwehand ◽  
Seppo Salminen ◽  
Erika Isolauri

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Riley Joel Steed

Since the second half of the 20th century, the incidence of atopic disease has been on the rise. Allergies and rhinitis have become so common that some have called it an epidemic (Strachan, 1989). Initial research into the reasons for the rapid increase was done by David P Strachan, and he proposed the “hygiene hypothesis,” a theory claiming that early childhood infections can protect us against atopic diseases later in life (Strachan, 1989). Subsequent research found an interaction between T-helper 1 and T-helper 2 cells that, for many years, was considered to be the mechanism by which the hygiene hypothesis functioned (Romagnani, 1992). Eventually, it was discovered that this interaction did not work exactly as previously thought, and Graham A. Rook introduced a new theory to match the more recent research. Rook proposed the “old friends” hypothesis, which suggested that certain microbes, which evolved alongside humans, were responsible for protecting us against atopic disease (Rook et al., 2004). According to Rook, modern lifestyles have eliminated many of those microbes from our normal flora, and that explains the recent rise in atopic disease (Rook et al., 2004). The “old friends” hypothesis is now the prevalent atopic disease theory in epidemiology, and has helped improve both public and scientific understanding of the relationship between infection, hygiene, and atopy (Stiesma, et al., 2015).


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