PubMed Health⌕ Search

PubMed · 3714096

[Iodine and delayed immunity].

Abstract

Iodine was and is sometimes used therapeutically in various pathologies where the immune mechanism is known to play a dominant role. It has in fact been administered to patients with tubercular granulomatous, lepromatous, syphilitic and mycotic lesions where it facilitates cure. This effect does not depend on iodine's action on the micro-organism responsible. Iodine may also be used in Villanova-Panol Panniculitis, in erythema nodosum, in nodular vasculitis, erythema multiforme and Sweet's syndrome. Oral iodine is also very effective in the lymphatic-cutaneous form of sporotrichosis. In order to establish a relationship between dietary iodine and immune response, 607 infants residing in an area of endemic goitre were studied: 215 were given Lugol solution (2 drops a week for about 8 months) and 392 not. The immune response was assessed by the skin test method using tetanic toxoid and a clear correlation was shown between this and lymphocyte stimulation and monocytic chemotaxis tests. The test was considered positive when an infiltration of at least 5 mm in diameter was shown after 48 hours (in the U.S. 80% of paediatric cases aged 2-10 years old were positive). A significant difference was noted in the average diameter of the infiltrations after the tetanic toxoid skin test in the two groups considered (P less than 0.001). The results appear to indicate that an adequate iodine intake is necessary for normal retarded immune response. The molecular mechanism by which iodine increases immune response is still to be decided.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

L Marani, S Venturi. 1986-05-07. [Iodine and delayed immunity].. https://pubmed.ncbi.nlm.nih.gov/3714096/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Synthesis, conformation and biological activity of centrally modified pseudopeptidic analogues of For-Met-Leu-Phe-OMe.

For-Met-betaAlapsi[CSNH]-Phe-OMe (3), For-Met-betaAlapsi[CH2NH]-Phe-OMe (5), For-Met-NH-pC6H4-SO(2-Phe-OMe 8a), For-Met-NH-mCH4-SO2-Phe-OMe (8b) and the corresponding N-Boc precursors (2, 4, 7a, b) have been synthesized and their activity towards human neutrophils has been evaluated in comparison with that shown by the reference tripeptide For-Met-Leu-Phe-OMe (fMLF-OMe). Chemotaxis, lysozyme release and superoxide anion production have been measured. (1)H NMR titration experiments and IR spectra have been discussed in order to ascertain the preferred solution conformation adopted by the tripeptide 3 with particular reference to the presence of a folded conformation centred at the centrally positioned thionated beta-residue.

Chemotaxis, Leukocyte↗

Molecular mechanism of nitrogen mustard induced leukocyte(s) chemotaxis.

Nitrogen mustard(s) (NM) are the primary chemotherapeutic agents (Chlorambucil, BSO) that are used in treating the B-cell chronic lymphocyte leukemia (B-CLL). It is known that NM imparts oxidative stress by inducing the reactive oxygen species (ROS) and reactive nitrogen species (RNS) production in B-lymphocytes of B-CLL. It is likely that these nitrogen mustards can cause the oxidative stress in the peripheral blood leukocytes (PBL) of B-CLL patients. It is possible that chronic exposure of PBL to NM would induce drug resistance in B-CLL patients. However, the precise molecular mechanism(s) by which NM affect the PBL are not known at present. Here, an effort is made to present plausible mechanisms by which chronic NM exposure could lead to increased PBL chemotaxis and vascular tissue damage in B-CLL patients The clinical implication of this phenomenon is most likely the unwanted organ dysfunction in B-CLL patients. Identification of viable therapeutic targets to attenuate the PBL activation during the NM therapy would be beneficial for the clinical remission of B-CLL.

Chemotaxis, Leukocyte↗

Intrauterine neutrophil activation is associated with pulmonary haemorrhage in preterm infants.

BACKGROUND: Clinical and experimental studies showing lung damage associated with biologically active neutrophil derivatives suggests the possibility that intrauterine neutrophil activation may predispose to the development of pulmonary haemorrhage in extremely low birthweight infants early after birth. OBJECTIVES: To assess neutrophil functional activity in cord blood from extremely low birthweight infants who subsequently developed severe pulmonary haemorrhage. METHODS: Neutrophil functional activity was evaluated in the cord blood of preterm neonates (gestational age <28 weeks and weight <800 g) who developed pulmonary haemorrhage (n = 6) and in controls who did not (n = 6). Infants with congenital abnormalities and noteworthy maternal complications such as diabetes, pre-eclampsia, haemorrhagic disorders, and connective tissue disease were excluded. Neutrophils isolated from cord blood immediately after delivery were tested to evaluate neutrophil chemotaxis, random motility, and chemiluminescence. Standard methodology was used. RESULTS: Chemotaxis and chemiluminescence of neutrophils from cord blood of infants with pulmonary haemorrhage was higher than in the controls (34.8 (2.0) v 28.6 (0.8) microm, p<0.001, and 95.8 (8.5) v 73.2 (3.6) cpm x10(3), p<0.001 respectively). Random motility of cord blood neutrophils was comparable in the two groups (28.6 (1.2) v 25.3 (1.2) microm, p<0.09). CONCLUSIONS: Intrauterine induction of chemotactic activity and metabolic oxygenation of neutrophils may predispose to the development of pulmonary haemorrhage in extremely low birthweight infants with respiratory distress early after birth.

Chemotaxis, Leukocyte↗