In lungs, clearance of organisms is mediated by innate immunity, specifically alveolar macrophages [30].
At the alveolar site pulmonary innate immunity is ensured by airway epithelial cells, alveolar epithelial cells (AEC) type I and II and alveolar macrophages that cofunction with surfactant-associated proteins belonging to the C-type lectin superfamily as well as antimicrobial peptides.
Furthermore, substances that directly affect alveolar macrophages can therefore affect immunity in the infant lung.
Although the underlying pathogenetic mechanisms are not fully understood, exposure to common gaseous pollutants affects the susceptibility to and the progression of infectious diseases through the impairment of local bronchial immunity, the modification of alveolar macrophages function and the epithelium damage [11].
The combination of ARDS-associated alveolar damage and associated local immune dysregulation [27], together with sepsis-induced immunosuppression [28], might, through alterations in innate immunity and antigen presentation processes [29], account for the development of IPA in previously colonized patients.
Thus, TLR2 recognition of mycoplasma respiratory infections by alveolar macrophages and other cells conferring innate immunity leads to clearance and/or control of these organisms in the lungs, but does not have a similar effect in nasal passages in this same period.
These effects include inhibition of cell membrane repair, impairment of alveolar fluid clearance, and suppression of innate immunity and host defense [ 19].
In summary, alveolar macrophages are critical regulators of Th2 immunity and their dysregulation promotes an inflammatory environment with exacerbation of allergen-induced airway pathology.
As mentioned previously, alveolar macrophages are key components of both innate and acquired immunity against invading pathogens in the lung.
Effects on levels of proteins in pathways associated with innate immunity, oxidative stress and apoptosis were evaluated in alveolar type II cell lysates by enzyme-linked immunosorbent assay.
