TNF-alfa induced apoptosis of acini in NOD submandibular glands: modulation by VIP

MARIO CALAFAT; LAROCCA L; ROCA V; PEREZ LEIROS C

Congreso; VII Congreso de la Sociedad Internacional de Neuroinmunomodulación (ISNIM); 2008

NOD mice are a suitable model of an autoinmmune exocrinopathy similar to Sjögren syndrome, characterized by histological and functional alterations of exocrine glands. It is proposed that a functional failure and/or inappropriate apoptosis in salivary glands could initiate the autoimmune response. We reported an increased apoptosis of acinar cells from NOD glands and high levels of serum TNF-α. VIP (vasoactive intestinal peptide) is an anti-inflammatory and prosecretory neuropeptide common to the nervous and immune systems. Our goal was to evaluate the involvement of TNF-α in early apoptosis of acini isolated from submandibular glands of NOD mice and the possible regulation by VIP. Acini from prediabetic NOD females (16 weeks old) were used for apoptosis determination and bax expression. TNF receptor1 and TP53INP1 were determined by RT-PCR and Western Blot. Our results indicate that TNF-α induced apoptosis in a concentration-dependent manner with a higher percentage at 5 ng/ml in NOD acini vs. control BALB/c. It also increased bax expression (arbitrary units of area-UA: X ± SE; Basal 51 ± 4; TNF 107 ± 5 P