Since biofilm formation may be associated with resistance to immune host response, many clinically significant bacterial species have been studied for their capacity to form biofilm [20].
As a second layer of the innate immune response, many host plant lineages evolved intracellular R-proteins of the NB-LRR type that respond to virulence factors, either directly or through their effects on host targets [ 6].
Of importance to the modeling of IBD, the antimicrobial roles of NOD1 and NOD2 are conserved in zebrafish (Oehlers et al., 2011c; Oehlers et al., 2011b), as are many aspects of the host response to microbial colonization, including intestinal alkaline phosphatase expression and NFκB activation (Bates et al., 2007; Kanther et al., 2011).
NETs have emerged as key players in the innate host response to many bacteria.
Many terminally located genes are host response modifiers that directly interact with components of the host immune response or cellular response to infection.
GO and pathway enrichment studies can detail many key aspects of the host response, but these biological functions and processes must be integrated to create host response models capable of linking the effects of transcription to the molecular and signaling events driving those effects.
The fact that IgM-RF positivity increases with age in non-RA but not in RA supports the notion that low-affinity RFs associated with infection and older age appear to play an important role in the host response to many infectious organisms and are likely to contribute to host defence.
In fact many pathogens manipulate host responses through direct and indirect interactions between pathogen and host proteins.
See related commentary: Many of the host responses to sepsis are similar to those seen after major injury, with increased energy expenditure (EE), enhanced protein catabolism [ 1- 3], increased use of lipids as oxidative fuel, and impaired glucose metabolism [ 4].
