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Iodine Research

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                            Iodine and the Body

Immune System (continued pg 2)

Myeloperoxidase-mediated iodination by granulocytes. Intracellular site of operation and some regulating factors.
Root RK, Stossel TP.
J Clin Invest. 1974 May;53(5):1207-15.

The intracellular site of operation of the myeloperoxidase-H2O2-halide antibacterial system of granulocytes has been determined by
utilizing measurements of the fixation of iodide to trichloracetic acid (TCA) precipitates of subcellular fractions, including intact
phagocytic vesicles. Na-125I was added to suspensions of guinea pig granulocytes in Krebs-Ringer phosphate buffer, and they were
then permitted to phagocytize different particles. Phagocytic vesicles were formed by allowing cells to ingest a paraffin oil emulsion
(POE) and collected by flotation on sucrose after homogenization. Measurement of 125I bound to TCA precipitates of the different
fractions and the homogenates disclosed that the lysosome-rich fraction obtained by centrifugation from control (nonphagocytizing)
cells accounted for a mean 93.1% of the total cellular activity. With phagocytosis of POE, TCA-precipitable iodination increased two-
to sevenfold, and the lysosomal contribution fell to a mean 36.9% of the total. The appearance of activity within phagocytic vesicles
accounted for almost the entire increase seen with phagocytosis (a mean 75.7%), and iodide was bound within these structures with
high specific activity. More iodide was taken up by cells than fixed, regardless of iodide concentration, and was distributed widely
throughout the cell rather than selectively trapped within the vesicles.

The amount of iodide taken up and fixed varied considerably with the phagocytic particle employed. Yeast particles were found to
stimulate iodination to a far greater degree than the ingestion of POE or latex. Such observations are consistent with the concept that
the ingested particle is a major recipient of the iodination process. Measurements of metabolic activities related to the formation and
utilization of peroxide by cells phagocytizing different particles were made and correlated with iodination. The findings suggest that
mechanisms must exist within granulocytes to collect or perhaps even synthesize H2O2 within phagocytic vesicles to serve as substrate
for myeloperoxidase. The simultaneous stimulation of other metabolic pathways for peroxide disposal and its release into the medium
by phagocytizing cells is consistent with the high diffusability of this important bactericidal substance.

[Iodine and delayed immunity]
Marani L, Venturi S.
Minerva Med. 1986 May 7;77(19):805-9.
[Article in Italian]  [abstract only]

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.

Accelerated cellular uptake and metabolism of L-thyroxine during acute Salmonella typhimurium sepsis.
DeRubertis FR, Woeber KA.
J Clin Invest. 1973 Jan;52(1):78-87.

The effects of acute Salmonella typhimurium sepsis on the kinetics of peripheral L-thyroxine (T4) distribution and metabolism and on
serum total and free T4 concentrations were studied in rhesus monkeys inoculated i.v. with either heat-killed or viable organisms. The
rate of disappearance of labeled T4 from serum was increased within 8 h after inoculation of monkeys with either heat-killed or viable
Salmonella. The effects of the heat-killed organisms were transient and no longer evident by 16 h postinoculation. The monkeys
inoculated with the viable Salmonella experienced a 2-3 day febrile, septic illness that was accompanied by an increase in the
absolute rate of T4 disposal. In the infected monkeys, serum total T4 and endogenously labeled protein-bound iodine concentrations
fell significantly during the period of acute sepsis and then rose during convalescence to values that exceeded the preinoculation
values, suggesting that thyroidal secretion of hormone had increased in response to a primary depletion of the peripheral hormonal
pool. Total cellular and hepatic uptakes of T4 were enhanced by 4 h after inoculation of monkeys with either heatkilled or viable
Salmonella, but the increase in total cellular uptake persisted for 24 h only in the monkeys inoculated with the viable organisms.
These alterations in T4 kinetics could neither be correlated with changes in the binding of T4 in plasma nor attributed to an increase
in vascular permeability. Moreover, they could not be ascribed to an in vitro product of bacterial growth, suggesting that the presence
of the organisms themselves was required. An acceleration of T4 disappearance was also observed during Escherichia coli and
Diplococcus pneumioniae bacteremias. Our findings are consistent with a primary increase in the cellular uptake and metabolism of
T4 during bacterial sepsis, possibly related to phagocytic cell function in the host.

Metabolism of L-thyroxine by phagocytosing human leukocytes.
Woeber KA, Ingbar SH.
J Clin Invest. 1973 Aug;52(8):1796-803.

Intact normal human leukocytes deiodinated L-thyroxine (T4) with the generation of inorganic iodide, chromatographically immobile
origin material, and small quantities of L-triiodothyronine (T3). When phagocytosis was induced in the leukocytes through the addition
of zymosan particles that had been opsonized by coating with plasma, T4-deiodination was greatly stimulated. In addition to the
stimulation of T4-deiodination, the accumulation by the leukocytes of undegraded T4 was increased. Anoxia, which has previously
been shown not to interfere with phagocytosis, did not prevent the increased cellular accumulation of T4 that phagocytosis induced,
but virtually abolished T4-deiodination. On the other hand, calcium, which has previously been shown to be required for optimal
phagocytosis, was required for the increase in both the cellular accumulation and deiodination of T4 that phagocytosis induced.
Phospholipase-C, which has previously been shown to induce a metabolic burst that mimics that induced by phagocytosis, did not
increase the cellular accumulation or deiodination of T4. On the other hand, colchicine, which has previously been shown to depress
the metabolic burst that accompanies phagocytosis, did not prevent the increase in either the cellular accumulation or deiodination
of T4 that phagocytosis induced. Thus, increased accumulation of T4 by the leukocytes during phagocytosis appears to be the
primary factor responsible for the stimulation of deiodination that phagocytosis induces. The increased accumulation of T4 did not
appear to be owing to engulfment of suspending medium surrounding the particles or to binding of T4 to the particles themselves. In
addition to the enhanced cellular accumulation, other factors related to the metabolic burst that accompanies phagocytosis might
also be involved in the stimulation of T4-deiodination. In leukocytes from two patients with chronic granulomatous disease, a disorder
in which phagocytosis appears to occur normally but in which the metabolic burst and attendant increase in hydrogen peroxide
generation do not occur, stimulation of T4-deiodination was either greatly diminished or totally lacking. In myeloperoxidase-deficient
leukocytes, on the other hand, stimulation of T4-deiodination was at least as great as that in normal cells. Thus, we conclude that the
primary factor responsible for the increased deiodination of T4 that phagocytosis induces is the enhanced cellular uptake of hormone.
The increased generation of hydrogen peroxide that accompanies phagocytosis may be necessary for the enhanced deiodination of
the accumulated T4, but the latter reaction does not require the mediation of myeloperoxidase.

Evidence for enhanced cellular uptake and binding of thyroxine in vivo during acute infection with Diplococcus pneumoniae.
DeRubertis FR, Woeber KA.
J Clin Invest. 1972 Apr;51(4):788-95.

Previous work has demonstrated that acute pneumococcal infections in man and in the rhesus monkey are accompanied by
accelerated metabolic disposal of L-thyroxine (T4). In order to study the influence of acute pneumococcal infection on the kinetics of
hormone distribution, the early cellular uptake of T4 (CT4), reflecting the net effect of plasma and cellular binding factors, was
assessed in rhesus monkeys....Thus, in the infected monkeys CT4 and% FT4 were not significantly correlated. The increased CT4 in
the infected monkeys could not be ascribed to an increase in vascular permeability and did not correlate with the magnitude of fever.
Although the increased CT4 could not be accounted for by increased hepatic or renal uptake of hormone, hepatic and renal T4
spaces were increased, results consistent with increased binding by these tissues. Our data indicate that the cellular uptake of T4 is
increased early in acute pneumococcal infection and suggest that this results from a primary enhancement of cell-associated binding
factors for T4.

Alterations in thyroid hormone economy during acute infection with Diplococcus pneumoniae in the rhesus monkey.
Woeber KA.
J Clin Invest. 1971 Feb;50(2):378-87.

In order to study the alterations in thyroid hormone economy that accompany an acute bacterial infection, rhesus monkeys were
inoculated i.v. with a virulent Diplococcus pneumoniae culture containing approximately 108 organisms per dose. This was found to
produce a well-defined febrile illness followed in most instances by spontaneous recovery, thereby permitting sequential observations
to be made during progression from the healthy state through acute infection into convalescence. During the acute febrile period of
the infection, the clearance of both exogenously labeled L-thyroxine (T4) and 3,3Œ,5-triiodo-L-thyronine (T3) from their peripheral
pools was accelerated. This alteration was often evident by 8 hr after inoculation with the virulent culture and could not be ascribed to
a decrease in extracellular binding. Despite the accelerated hormonal clearance, the concentrations of both endogenously labeled
thyroid hormone and stable T4 in the sera of the surviving monkeys remained essentially unchanged or increased, indicating that
hormonal secretion must have increased during this period. During the convalescent period, hormonal clearance was similar to
preinfection control values. Leukocytes isolated from blood obtained 6 hr after inoculation with the virulent culture displayed
enhanced T4-deiodinative activity.