# PMN LEUKOCYTE MOTILITY & ADHESIVE PROPERTIES IN NEONATES

> **NIH NIH R01** · BAYLOR COLLEGE OF MEDICINE · 1988 · $134,472

## Abstract

Human neonates and individuals with heritable Mac-1, LFA1 deficiency are at
high risk for the development of infectious complications resulting from
impaired tissue mobilization of phagocytic cells.  These studies will
evaluate pathogenic mechanisms that may account for impaired PMN or
mononuclear leukocyte mobilization in these populations.  Major emphases
will include determinations of:  a) functional relationships between
cellular adherence and migratory properties, b) mechanisms regulatin the
induction, modulation and functional activation of cellular adherence by
inflammatory stimuli, and c) possible pathologic influences of cytoskeletal
proteins (microtubules) on cell translocation.  They will focus on the
contributions of a family of "adhesive" glycoproteins (GPs) (Mac-1, LFA1,
p150,95) to adherence-dependent properties of leukocytes; comparative
studies employing neonatal and Mac-1 deficient cells will allow a unique
opportunity to understand functional and clinical consequences of abnormal
expression.  Surface expression of Mac-1 GP when mediated by chemotactic or
secretory stimuli will be quantitated using immunofluorescence flow
cytometry and 125I immunoprecipitation techniques employing monoclonal
antibodies (MAb); their topographical relationships to other surface
reptors (FcR and CR1) and to "adhesion sites" will be evaluated by IIF
microscopy.  MAbs to each Mac-1 subunit will be employed in blocking
experiments to assess their functional contributions to adhesion-dependent
cell functions including microtubule and microfilament assemblage (IIF
tubulin and actin probes).  The relationships of Mac-1 GP "up regulation",
hyperadherence and secretory events will be studied and possible secretory
determinants of impaired Mac-1 GP induction and hyperadherence of neonatal
PMNs will be assessed.  Subcellular fractionation and a new concanavalin A
binding assay will be employed to determine the location of intracellular
Mac-1 pools and to evaluate mechanisms regulating their surface expression,
redistribution and/or recycling.  Selected pathogenic mechanisms accounting
for disturbed MT assembly of neonatal PMN including:  abnormal cell
adherence-dependent cytoskeletal activation, abnormal post-translational
tubulin tyrosylation, or intrinsic immunochemical abnormalities of or Alpha
or Beta tubulin will be evaluated with intracellular immunofluorescence
probes under conditions promoting MT assembly or disassembly.  These
studies should provide a basis for understanding the functional and
clinical consequences of disturbed adhesion-dependent cellular functions in
the inflammatory response, and potentially allow the development of
therapeutic strategies in these and other high risk pediatric models.

## Key facts

- **NIH application ID:** 3128443
- **Project number:** 5R01AI019031-07
- **Recipient organization:** BAYLOR COLLEGE OF MEDICINE
- **SAM.gov UEI:** FXKMA43NTV21
- **Principal Investigator:** Donald C. Anderson
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1988
- **Award amount:** $134,472
- **Award type:** 5
- **Project period:** 1982-04-01 → 1989-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3128443

## Citation

> US National Institutes of Health, RePORTER application 3128443, PMN LEUKOCYTE MOTILITY & ADHESIVE PROPERTIES IN NEONATES (5R01AI019031-07). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3128443. Licensed CC0.

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