[PubMed] [Google Scholar] Zimmer WM, Rogers RS, III, Reeve CM, Sheridan PJ. levels and antibodies to whole cells of and were assayed by enzyme-linked immunosorbent assay (ELISA) in serum, whole saliva and parotid saliva. Serum IgA and IgA1 and IgA2 subclasses were raised in all patient groups (< 001). Salivary IgA (and IgG) levels were raised in OFG and OFG + CD (< 001) but not in the CD group. Parotid IgA was also raised in OFG and OFG + CD but not in CD. The findings suggest that serum IgA changes reflect mucosal inflammation anywhere in PI-103 the GI tract but that salivary IgA changes reflect involvement of the oral cavity. Furthermore, the elevated levels of IgA in parotid saliva suggest involvement of the salivary glands in OFG. Serum IgA antibodies to were raised markedly in the two groups with gut disease while serum IgA (or IgG) antibodies to were elevated significantly in all three patient Rabbit polyclonal to TrkB groups (< 002). No differences were found with antibodies to (and may reflect gut inflammation while raised SIgA antibodies to or raised IgA or IgA2 levels in saliva reflect oral but not gut disease. Analysis of salivary IgA and IgA antibodies to as well as serum antibodies in patients presenting with OFG may allow prediction of gut involvement. Keywords: antigens in CD [9C12]. The significance of this PI-103 finding remains uncertain but the presence of IgA anti-antibodies has been proposed as a means of distinguishing between CD and other types of inflammatory bowel diseases [13]. The cause of OFG is unknown in most patients. Thus agents suggested as being possibly associated with CD are of particular interest. These include antigens from [14C17] and from a common dietary component, [12,13]. Studies have shown elevated serum titres of both IgG and IgA to in CD patients compared with ulcerative colitis patients and healthy controls [11C13]. It had been suggested that serum IgA anti-may be a highly specific serological marker for CD [11,12]. An unconfirmed case PI-103 report [18] has also implicated as a possible aetiological agent in MRS. The aim of this study was to provide further PI-103 insight into the relationship between OFG and CD and to determine whether OFG could be distinguished immunologically from CD. nonspecific and specific aspects of humoral immunity (serum and salivary antibodies to = 14, age range 12C73 years, mean 386 69); (b) those with CD and with OFG signs (OFG CD group) including patients presenting with OFG and in whom evidence of intestinal pathology consistent with CD was found on colonoscopy (= 12, age range 10C55 years, PI-103 mean 283 7); and (c) CD patients with no detectable oral signs (CD group) (= 22, age range 21C70 years, mean 467 74. With the exception of the CD group, in which there were 14 males and eight females, the other groups showed an even male/female distribution. Serum samples Venous blood samples were collected during routine patient consultations and following centrifugation of the clotted blood, several aliquots were taken and stored at ?70C. Control serum samples were obtained from staff and patients referred to the Department of Oral Medicine and Pathology, Guy’s Hospital. None had been referred for assessment of conditions likely to be related to increased carriage of or other fungal organisms, or for ulcerative conditions. As far as possible they were age- and sex-matched to the entire patient group, which had an age range from 10 to 72 years with a mean of 384 42 (s.e.m.). A total of 29 sera were selected from controls with an age range of 10C73 years, mean 379 36 (s.e.m.). Saliva samples Unstimulated whole saliva was collected in sterile universal containers, and 50 l cultured on standard Sabouraud’s dextrose agar at 37C for 48 h. The remainder was centrifuged and several aliquots stored at ?70C until required. Stimulated parotid saliva was collected over 10 min in all patients and controls from the right parotid duct as described previously [19]. Ten of the control subjects and 12 of the patient group showed salivary carriage of but all had.
