Conjugated linoleic acids (CLA) are a family of more than two dozen isomers of linoleic acid. They are synthesized by the microbes during fatty acid biohydrogenation in the rumen. Therefore, foods of ruminant origin, such as dairy, beef, mutton, and chevon products are the primary sources of CLAs. Although one of the essential nutrients, fats in general are perceived to have negative health effects. However, research has shown that CLAs are highly beneficial for our health, at least as shown in many experimental cell culture and animal research models. Of all the isomers, c-9, t-11 and t-10, c-12 CLAs are the primary ones deemed important from health perspective. Moreover, these are the only ones that are present in ruminant foods in any appreciable amounts. In general, food products from grass-fed ruminants are good sources of CLA, and contain much more of it than those from grain-fed animals.
Effect of CLA on immunomodulation is also emerging slowly. It has been demonstrated that the two active CLA isomers (c-9, t-11 and t-10, c-12 CLAs) can elicit both the innate and adaptive immune responses (Albers et al., 2003; O’Shea et al., 2004; He et al., 2007). Sugano et al. (1999) initially proposed that the immune enhancing effect of CLA was by modulating eicosanoid and immunoglobulin production, which were later affirmed by other investigators (Cheng et al., 2003; Ramakers et al., 2005; Ringseis et al., 2006), as well as the ability of CLAs to modify cytokines (Hur et al., 2007). Indeed, Song et al. (2005) investigated the effect of dietary CLA supplementation (3 g/day; 50:50 mixture of c,9, t-11 and t-10, c-12 CLA isomers) on the immune system of healthy human (male and female) volunteers. It was found that the levels of plasma immunoglobulins (Ig) A and M were increased with decreased plasma levels of E. CLA supplementation also decreased the levels of the proinflammatory cytokines, TNF-α and IL-1β, but increased the levels of anti-inflammatory cytokine, IL-10.
Enhanced immune function is usually associated with anorexia and wasting. In a detailed review, Cook et al. (2003) showed that CLA not only enhances immune response, but also protects tissues from collateral damage. CLA also diminished lipopolysaccharide-induced inflammatory events in macrophages through reduced mRNA and protein expression of nitric oxide synthase and cyclooxigenase-2 as well as subsequent production of nitric oxide and prostaglandin E2 (Cheng et al., 2004), both of which are also implicated in carcinogenesis. Cook et al. (1999) suggested that CLA prevents immune associated wasting by protecting nonlymphoid tissues from the adverse effects of cytokines, which are growth suppressants, because CLA influences the immune system by altering the effects of cytokine, interleukin, leukotriene and many immunoglobulins (Sébédio et al., 2000). Although dietary CLA enhanced antibody production in broiler chickens (Takahashi et al., 2003), ameliorated viral infectivity in a pig model of virally induced immunosuppression (Bassaganaya-Riera et al., 2003), and enhanced lymphocyte proliferation in nursery pigs (Bassaganaya-Riera et al., 2001), no change in immune status was observed in young healthy women (Kelley et al., 2000). Whigham et al. (2002) indicated that CLA might induce a change in immune response in favor of cell-mediated response rather than an allergic one, while Nichenametla et al. (2004) showed higher natural killer cell cytotoxicity in rats fed CLA in diet than the control group without CLA. It appears that c-9, t-11 and t-10, c-12 isomers of CLA stimulate different immunological events in mice with c-9, t-11 increasing tumor necrosis factor α while t-10, c-12 increasing immunoglobulin A and M production (Yamasaki et al., 2003).
Foregoing in vitro studies demonstrate that CLA modulate immune function. In a double blind parallel reference-controlled intervention study in adult humans, almost twice as many subjects reached protective antibody levels to hepatitis B when consuming a 50:50 mixture of c-9, t-11 and t-10, c-12 CLA isomers for 12 weeks compared with sunflower oil fed reference subjects, but the response to 80:20 mixture of c-9, t-11 and t-10, c-12 CLA was similar to that of reference (Albers et al., 2003). This is probably the first of its kind about the effects of CLA on immune function using actual human subjects. In contrast, CLA feeding to young healthy women did not alter any of the indices of immune status tested (Kelly et al., 2000). Recently, Kwak et al. (2009) observed in obese pre-menopausal Korean females that CLA (c-9, t-11 and t-10, c-12 CLA mixture) supplementation modulated the increased release of markers (C-reactive protein, IL10, IgM) related with inflammation and immune function, and this effect was much more subtle than those found in animals and few other clinical studies.
To date there have been limited attempts at identifying the effects of specific isomers of CLA on the immune system. In one such study, CLA (80:20 c-9, t-11:t10, c12) supplementation at 1% diet administered from gestation to adulthood enhanced specific systemic cell-mediated immunity as well as the mucosal IgA immune response, whereas it downregulated the polyclonal activation of the immune system suggesting the long-term effects of probably c-9, t-11 CLA isomer on the immune system (Ramirez-Santana et al., 2009). In another study, Whigham et al. (2000) concluded that t-10, c-12 isomer competitively inhibited the conversion of arachidonic acid to prostaglandin E2, a principal mediator of inflammation in diseases such as rheumatoid arthritis and osteoarthritis.
While the positive effects of CLA in cell culture and animal models appear encouraging, not very many studies in humans have been conducted. As a result, more such studies are needed to ascertain the effects of individual isomers of CLA or their mixtures.
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