Agriculture Reference
In-Depth Information
specificity between milk and intestine IgA (Salmon, 2000). Piglets begin to synthetize
their secretory IgA from the second week of age (Allen
et al.
, 1973).
15.2.7
Innate immunity
The innate immunity of the gut resides in preventing pathogens from going from the
lumen to the lamina propria, and thereby the bloodstream of piglets. The mucosal
barrier develops several extrinsic mechanisms such as peristalsis, proteolysis, acid pH,
and gastrointestinal flux. The epithelium itself also produces antimicrobial peptides
(cathelicidins and defensins) and enzymes (intestinal alkaline phosphatase) that limit
bacterial transepithelial passage and detoxify pro-inflammatory lipopolysaccharides
(LPS). The presence of the epithelial mucus layer with secretory IgA is an important
aspect of intestinal protective immunity not only by protecting against colonization
and invasion of pathogenic microorganisms (high-affinity IgA) but also, by confining
commensal bacteria in the intestinal lumen through a process known as 'immune
exclusion' (low-affinity IgA). Other mechanisms involve the presence of innate
sensing receptors expressed by enterocytes or underlying dendritic cells. These are the
pattern recognition receptors, including TLR and the intracellular nucleotide-binding
oligomerization domain (NOD)-like receptors that recognize bacterial components,
and the retinoic-acid-inducible gene I (RIG-I)-like helicases which are sensors for
virus. These receptors initiate the innate immune response and regulate the adaptive
response to infection or tissue injury. Binding of bacteria or bacterial components to
pattern recognition receptors (surface or intracellular) activates the NF-κB pathway with
downstream transcription of pro-inflammatory cytokines. Nevertheless, early after birth,
other mechanisms enable commensal bacteria to be tolerated in order to strictly regulate
exaggerated activity in the gut. Postnatally, pattern recognition receptors become poorly
accessible on the apical surface of epithelial cells and the action of TLR, that were initially
activated by commensal bacteria, could be dampened by negative regulators of their
expression produced by intestinal epithelial cells (Abreu, 2010).
15.2.8
Adaptive immunity
The balance between Th1 and Th2 responses in neonatal mice and young infants is skewed
toward a Th2 profile, resulting in high susceptibility to intracellular pathogen infection
(Adkins
et al.
, 2004). It has been demonstrated that neonates are not able to mount an
efficient immune response to a large number of pathogens because Th1 responses are
compromised at several steps, including deficient production of Th1-type cytokines by
CD4+ T cells and mononuclear phagocytes (Marodi, 2001). Age-related maturation
of the Th1/Th2 balance results in changes in cytokine secretion such as increased pro-
inflammatory IFNγ secretion, which is considered as a maturation marker of postnatal
mucosal immunity development. There have been several reports showing that the
expression of genes promoting IFNγ production is affected by intestinal bacteria. The
mRNA for porcine IL-17 is strongly expressed in mucosal tissue (Katoh
et al.
, 2004)
and, once again, commensal bacteria, more particularly segmented filamentous bacteria,
stimulate the development and accumulation of Th17 cells in gut mucosa (Niess
et al.
,
2008).
