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Biomedical subjects

M M D'Alesandro

Publications and source records attributed to M M D'Alesandro.

22 records · Page 2Linked to original sources
PubMed1987

Glucan: mechanisms involved in its "radioprotective" effect.

It has generally been accepted that most biologically derived agents that are radioprotective in the hemopoietic-syndrome dose range (eg, endotoxin, Bacillus Calmette Guerin, Corynebacterium parvum, etc) exert their beneficial properties by enhancing hemopoietic recovery and hence, by regenerating the host's ability to resist life-threatening opportunistic infections. However, using glucan as a hemopoietic stimulant/radioprotectant, we have demonstrated that host resistance to opportunistic infection is enhanced in these mice even prior to the detection of significant hemopoietic regeneration. This early enhanced resistance to microbial invasion in glucan-treated irradiated mice could be correlated with enhanced and/or prolonged macrophage (but not granulocyte) function. These results suggest that early after irradiation glucan may mediate its radioprotection by enhancing resistance to microbial invasion via mechanisms not necessarily predicated on hemopoietic recovery. In addition, preliminary evidence suggests that glucan can also function as an effective free-radical scavenger. Because macrophages have been shown to selectively phagocytize and sequester glucan, the possibility that these specific cells may be protected by virtue of glucan's scavenging ability is also suggested.

5'-Nucleotidase↗
PubMedDate not supplied

Alteration of rat polymorphonuclear leukocyte function after thermal injury.

One portion of host defense to bacterial challenge(s) involves the activation and infiltration of endogenous polymorphonuclear leukocytes. Thermal injuries are frequently associated with immunologic abnormalities including alterations of polymorphonuclear leukocyte-associated nonspecific resistance. We examined isolated peripheral rat polymorphonuclear leukocytes for alterations in membrane potential, oxidative capability, and locomotor function after the experimental application of 20% full-thickness body surface area thermal injury. Thermal injury resulted in significant reductions of peripheral red blood cell concentration(s) and increases in leukocyte and platelet concentrations for 42 days after injury. In addition to the quantitative changes, polymorphonuclear leukocytes also demonstrated altered qualitative functions. Compared with phorbol myristate acetate-induced activation of normal cells, polymorphonuclear leukocyte membranes from thermal-injured animals were electrophysiologically less responsive for 3 weeks after injury. The ability of polymorphonuclear leukocytes to produce intracellular H2O2, a measure of oxidative function, was also significantly decreased for 7 days after injury. The paradox in this paradigm of thermal injury was the demonstration of peripheral polymorphonuclear leukocyte quantitative increases with concurrent significant qualitative impairment. Qualitative lesions included altered states of membrane depolarization and depressed oxidative capability that may individually, or collectively, reduce nonspecific immune capabilities of the host to levels that are inadequate to combat infection.

Animals↗
PubMedDate not supplied

Quantitative and functional alterations of peripheral blood neutrophils after 10% and 30% thermal injury.

Polymorphonuclear leukocytes (PMNs) comprise the majority of early nonspecific inflammatory responses to infection or trauma and, as such, must be of sufficient number and qualitative function to properly limit and combat inflammation. Peripheral PMNs isolated from rats that received 10% or 30% body surface area full-thickness thermal injuries were quantitated and examined for functional alterations in membrane potential and cytosolic hydrogen peroxide production for 35 days after thermal injury. With 10% thermal injury, leukocytes increased quantitatively to experimental maximums that were 70% above normal on day 7 before a return to normal by day 28. Platelet levels showed a nonsignificant decrease for 2 days after thermal injury before increasing to levels 20% to 40% above normal through day 28. Phorbol myristate acetate-induced PMN membrane depolarization was inhibited as much as 30% for 21 days after 10% thermal injury. No changes in oxidative activity were apparent except for day 14, when hydrogen peroxide production was 40% above normal. With 30% thermal injury, leukocyte quantities were three to five times normal, with increased relative numbers of PMNs and decreased lymphocytes through day 28. Platelet levels decreased for 4 days before increasing to levels 30% to 47% above normal through day 21. Compared with 10% thermal injury, 30% thermal injury further reduced the ability of PMN membranes to depolarize through day 35. In addition, PMN hydrogen peroxide production was 30% lower on day 1 and increased thereafter to levels that were 40% above normal on day 21.

Animals↗