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Glutamine depletion potentiates leucocyte-dependent inflammatory events induced by carrageenan or Clostridium difficile toxin A in rats.
Nascimento, Silvia B. 1; Sousa, Romualdo B. 1; Martins, Marcos Jullian B. 1; Gomes, Antoniella Souza 1; Souza, Marcellus Henrique L. P. 1; Guerrant, Richard L. 4; Cunha, Fernando Q. 3; Ribeiro, Ronaldo A. 1; Brito, Gerly A. C. 2
[Article] Immunology. 116(3):328-336, November 2005.

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Summary: This research investigated the effect of glutamine (Gln) depletion on leucocyte-dependent inflammatory events. Rats were treated intraperitoneally, 16 hr prior to the peak of every parameter evaluated, with either 0[middle dot]9% NaCl, methionine-sulphoximine (MSO, an inhibitor of endogenous Gln synthesis, 25 mg/kg) or with MSO Gln (MSO as above plus Gln 3 g/kg in three doses). MSO-induced Gln depletion increased paw oedema induced both by carrageenan (Cg) and by Clostridium difficile toxin A (TxA) (66[middle dot]2% and 45[middle dot]5%, respectively; P < 0[middle dot]05). In dextran-injected animals, oedema and myeloperoxidase (MPO) activity were not modified by Gln depletion. In Cg-treated paws, Gln depletion increased MPO activity by 44% (P < 0[middle dot]05), interleukin-1[beta] (IL-1[beta]) and tumour necrosis factor-[alpha] (TNF-[alpha]) concentrations by 47% and 52%, respectively (P < 0[middle dot]05), and immunostaining for TNF-[alpha] in paw tissue. In TxA-injected paws, Gln depletion increased MPO activity (46%; P < 0[middle dot]05). Gln depletion increased Cg- and TxA-induced neutrophil migration to subcutaneous air pouches by 56% and 77% (P < 0[middle dot]05), respectively, but did not affect migration induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP). Gln infusions reversed all the effects of MSO. Leucocyte counts did not differ between groups. Gln depletion potentiates acute inflammation, possibly by increasing neutrophil migration through resident cell activation and production of IL-1[beta] and TNF-[alpha]. Gln supplementation reverses these effects and may be useful during inflammatory catabolic stress.