UTSA researcher receives grant to design vaccines

(Sept. 25, 2002)--University of Texas at San Antonio Assistant Professor of Immunology Bernard Arulanandam was recently awarded a $180,000 grant from the National Institutes of Health (NIH) to develop vaccine strategies for a host of diseases and to design therapeutic anti-inflammatory agents.

UTSA is ranked second among all institutions in the state of Texas for the amount of biology research funding it receives from the NIH. Nationally, UTSA is ranked No. 22 in research funding for biology out of 487 institutions of higher learning in the United States.

Arulanandam's laboratory will concentrate on nasal, non-invasive methods of providing immunization, due to the fact that most pathogens enter the host via mucosal membranes in the nasal passages. If bacteria or viruses are prevented from attaching to the mucosa they cannot spread throughout the body. The mucosal immune system, the body's first line of defense, must routinely differentiate between substances it should keep out (such as bacteria) versus those it should let in (such as vaccines).

Arulanandam research will focus on Staphylococcus aureus (S. aureus), a bacteria often associated with conditions such as septic arthritis and septicemia. Septicemia affects 70,000 to 300,000 individuals in the U.S. every year. Septic arthritis often leads to joint destruction, despite the use of antibiotics. Both conditions are often antibiotic resistant.

IgA (Immunoglobulin A), the major human immune system defense at mucosal sites, prevents bacteria from colonizing. Vaccines that augment IgA are very beneficial to humans. The connection between IgA and S. aureus is that individuals with IgA-deficiency have a greater predisposition to autoimmune conditions and to recurrent S. aureus infections. One of every 800 individuals is IgA-deficient.

Arulanandam will investigate this phenomenon using IgA-deficient animals and animals that do not transport IgA, which will provide information about how IgA in the blood and mucosa are different, and how they work to regulate infection.

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