Abstract
Milk is globally consumed as a rich source of protein and calcium. A major protein component of milk is casein, with β-casein having 2 major variants A1 and A2. Of these, A1 casein variant has been implicated as a potential etiological factor in several pathologies, but direct effect on lungs has not been studied. The objective of the present study was to evaluate the A1and A2 β casein variants of cow milk as factors causing allergic airway disease in murine model. Mice fed with A1A1 milk exhibited increased airway hyperresponsiveness with increasing concentration of bronchoconstrictor (methacholine), which was not observed in mice fed with A2A2 milk. Significantly elevated levels of IL-4 and IL-5 were found in bronchoalveolar lavage and serum of A1A1 variant fed mice. Increased IgE and IgG levels along with increased infiltration of lymphocytes and eosinophils, leading to peribronchial inflammation was also observed in A1A1 variant fed mice, although, no goblet cell hyperplasia or airway remodeling was observed. In contrast, A2A2 milk fed mice presented phenotype matching the control group, while A1A2 milk fed group presented an intermediate phenotype. In summary, our results show that A1 form of cow milk has a proinflammatory effect on the lung resulting in phenotype closely matching with the typical allergic asthma phenotype.
Highlights
Similar to its effects on gut inflammation, cow milk has been found to have immunomodulatory effects on respiratory health[15]
On assessing the same in our study, we found that the IgG levels in bronchoalveolar lavage (BAL) were significantly higher in mice fed with A1A1 milk as compared to the control as well as mice fed with A1A2 and A2A2 milk (Fig. 3b)
A recent study demonstrated that raw cow milk prevented house dust mite-induced airway inflammation in a murine asthma model[16]
Summary
Similar to its effects on gut inflammation, cow milk has been found to have immunomodulatory effects on respiratory health[15]. Feeding of mice with raw cow milk prevented airway inflammation in house dust mite-induced asthma model while processed milk did not; probably due to loss of some heat-labile components[16] As both pulmonary and gut inflammation are very similar, being Th2-driven and involving deregulation of mucosal immunity, it has been suggested that a subgroup of individuals with respiratory ailments involving mucus overproduction may benefit from elimination of dairy components from their diet[17], though a systemic investigation into underlying mechanisms hasn’t been performed yet. Long-term feeding of mice with A1A1 milk for around 30 weeks significantly increased methacholine induced airway hyperresponsiveness and was accompanied by increased recruitment of lymphocytes, eosinophils and total inflammatory cells in both bronchoalveolar lavage (BAL) and blood It was primarily a Th2 response, as suggested by increase in the Th2 cytokines i.e IL-4 and IL-5 with no significant difference in the levels of IFNγ which is Th1 cytokine; along with increased IgE in both BAL and serum and IgG levels in BAL. While A2A2 milk had no negative effects, with trends instead suggesting a protective role if any, feeding the mice with A1A2 milk produced intermediate inflammatory effects
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