Mucosal immunity

Vitamin A deficiency impairs mucosal function through several mechanisms: (i) loss of cilia in the respiratory tract; (ii) loss of microvilli in the gastointestinal tract; (iii) loss of mucin and goblet cells in the respiratory, gastrointestinal and genitourinary tracts; (iv) squamous metaplasia with abnormal keratinization in the respiratory and genitourinary tracts; (v) alterations in antigen-specific secretory immunoglobulin A (IgA) concentrations; (vi) impairment of mucosal-associ-ated immune-cell function; and (vii) decreased integrity of the gut. The first four were among the most striking findings described in early studies of vitamin A-deficient animals and humans (Wolbach and Howe, 1925; Blackfan and Wolbach, 1933; Sweet and K'ang, 1935). The ocular surface has also been intensively studied during vitamin A deficiency, and loss of mucin and goblet cells and squamous metaplasia of the conjunctiva and cornea are well known (McLaren, 1963; Sommer, 1982). There is a close relationship between vitamin A status and the expression of mucins (Koo et al., 1999; Tei et al., 2000) and keratins (Gijbels et al., 1992; Darwiche et al., 1993). Mucins are large glycocon-jugates that are found on cell surfaces and secreted into the lumens of the gastrointestinal, respiratory and genitourinary tracts. Mucins are also secreted on the bulbar and palpebral conjunctivae of the eye. The loss of mucin that occurs in vitamin A deficiency constitutes a serious impairment of mucosal immunity.

Table 8.1. Effects of vitamin A deficiency on host defence.

Abnormal expression of keratins in the respiratory tract, genitourinary tract and ocular surface Loss of cilia from respiratory epithelium Loss of microvilli from small intestine

Decrease in goblet cells and mucin production in mucosal epithelia Impaired neutrophil function

Impaired natural killer (NK) cell function and decreased number of NK cells

Impaired aspects of haematopoiesis

Shift towards T-helper type 1-like immune responses

Decrease in number and function of B lymphocytes

Impaired antibody responses to T-cell-dependent and independent antigens

In vitamin A-deficient chickens, the concentrations of total IgA were lower in the gut than in control animals (Rombout et al., 1992). Vitamin A-deficient BALB/c mice that were challenged with influenza A virus had a lower influenza-specific IgA response than control mice (Gangopadhyay et al., 1996). Vitamin A-deficient mice had significantly lower serum antibody responses against epizootic diarrhoea of infant mice (EDIM) rotavirus infection compared with control mice (Ahmed et al., 1991). An impaired ability to respond with IgA antibodies to oral cholera vaccine was demonstrated in vitamin A-deficient rats (Wiedermann et al., 1993a). Using the urinary lactulose/mannitol excretion test, increased gut permeability was found in vitamin A-deficient infants, and the gut integrity improved following vitamin A supplementation (Thurnham et al., 2000).

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