In endotoxemic mice, glutamine maintained B and T lymphocyte population in Peyer’s patches by preventing GSH reduction (Manhart et al. 2001). A single administration of glutamine was also able to enhance lymphocyte population both in intestinal (Lee et al. 2012; Tung et al. 2013) and lung (Hou et al. 2013; Hu et al. 2014) tissues by limiting T cell apoptosis.

In critical illness, alterations of immune function have been reported. In monocytes from trauma patients, glutamine parenteral supplementation restored HLA-DR expression that plays a critical role in the induction of the cellular immune response (Boelens et al. 2002). During acute pancreatitis, intravenous glutamine supplementation increased lymphocyte count (de Beaux et al. 1998). Thus, glutamine may improve cellular immune response in critical illness. Concerning innate immune response, experimental data revealed that glutamine may affect toll-like receptor activation, in particular, TLR4 (Mbodji et al. 2011; Ren et al. 2014). However, in trauma patients receiving glutamine, TLR4 and TLR2 on circulating monocytes remained not modified (Perez-Barcena et al. 2010).

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