# IMMUNOREGULATION OF GUT EPITHELIUM TO ESCAPE PARASITISM

> **NIH NIH R01** · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · 1988 · $206,183

## Abstract

Proposed research focuses on the interface between infective L1
larvae of Trichinella spiralis and the host at the level of the small
intestinal epithelium, the parasite's habitat.  The objective is to
test the hypothesis that physiological changes in epithelium,
mediated through an immunological reaction, are important in
effecting the rapid rejection of L1 larvae in rats and guinea pigs
undergoing a challenge infection.  Specific aims are to (a)
characterize small intestinal epithelial physiology in
nonimmunized and immunized rats and guinea pigs, (b) provide
evidence that an attempt by the L1 stage to penetrate tissue is
necessary to elicit epithelial responses in immunized hosts, (c)
provide evidence that epithelial changes elicited in immunized
hosts are mediated by an anaphylactic reaction, and (d) determine
the physiological characteristics of epithelium in immunized,
challenged hosts that are linked temporally and spatially with the
capacity to express rapid rejection.  Aims will be pursued using
several procedures to assess epithelial functions in alternative
hosts models.  Experimental designs will include as hosts (a)
uninfected rats and guinea pigs and their counterparts primed by
infection to express rapid rejection, (b) rats and guinea pigs
primed for expression of rapid rejection by inoculation with worm
antigens, (c) passively immunized rats and guinea pigs, (d) rats
treated with steroids to suppress rapid rejection, (e) athymic rats,
and (f) rats infected with parasites other than T. spiralis.
Alterations in epithelial function elicited by challenge with L1
larvae or their antigens used in neat form, incorporated into
liposomes or adhered to a heterologous parasite, will be
investigated.  Electrophysiological and isotope tracer
methodologies, cell fractionation procedures, lectin binding assays
and enzymatic analyses will be used.  Procedures will be employed
to study intestinal tissue in full thickness, isolated epithelial cells
and brush border and basolateral membranes of these cells.  Host
hypersensitivity will be gauged through passive cutaneous
anaphylaxis and Schultz-Dale reactions and an in vivo "equivalent"
of the Schultz-Dale reaction which involves monitoring infection-
induced myoelectric activity in conscious hosts.  The objective is
to define the physiological basis of acquired resistance to
infective larvae of T. spiralis.  Additionally, the project will lead
to the development of models for the study of
immunopathological and immunophysiological processes in
mucosal tissues down to the subcellular level.

## Key facts

- **NIH application ID:** 3124935
- **Project number:** 5R01AI011361-13
- **Recipient organization:** UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
- **SAM.gov UEI:** ZUFBNVZ587D4
- **Principal Investigator:** GILBERT A. CASTRO
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $206,183
- **Award type:** 5
- **Project period:** 1978-07-01 → 1991-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3124935

## Citation

> US National Institutes of Health, RePORTER application 3124935, IMMUNOREGULATION OF GUT EPITHELIUM TO ESCAPE PARASITISM (5R01AI011361-13). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3124935. Licensed CC0.

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