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Biomedical subjects

J F Jones

Publications and source records attributed to J F Jones.

At least 73 records · Page 4Linked to original sources
PubMed1984

Human polymorphonuclear-leukocyte inhibition of incorporation of chitin precursors into mycelia of Coccidioides immitis.

Human polymorphonuclear leukocytes (PMNLs), when added to arthroconidial suspensions of Coccidioides immitis, markedly inhibit fungal incorporation of the cell-wall precursor N-acetylglucosamine. This effect does not require serum but is facilitated by a heat-labile serum component(s), probably by promoting PMNL attachment to the arthroconidia. Inhibition is entirely reversible within 24 hr. In parallel with this finding, PMNLs exhibited virtually no killing of arthroconidia and (as determined by electron microscopy) did not produce damage to the fungal ultrastructure. PMNLs from a patient with chronic granulomatous disease suppressed fungal incorporation of N-acetyl-glucosamine by only 0%-22% under various conditions, as compared with 54%-85% suppression by PMNLs from normal donors. Our studies demonstrate that PMNLs can influence the metabolism of C immitis and raise the possibility that their presence in coccidioidal histopathology may be an important immediate host defense in limiting progression early after infection.

Acetylglucosamine↗
PubMed1984

In vivo analysis of impaired macrophage bactericidal capacity during experimental African trypanosomiasis.

Since innate resistance of mice to Salmonella typhimurium depends on an intact macrophage system, we have used this bacterium to investigate the effect of Trypanosoma brucei subsp. rhodesiense infection on macrophage phagocytic and cytolytic function. CBA/CaJ mice infected with T. brucei subsp. rhodesiense have decreased resistance to S. typhimurium, since doubly infected mice rapidly succumb to sublethal doses of S. typhimurium. Although trypanosomiasis is known to suppress antibody formation, such a suppression of antibody does not seem to play a role in trypanosome-induced sensitivity to S. typhimurium. A trypanosome-induced blockade of the reticuloendothelial system also does not occur, since parasitized and control mice clear S. typhimurium from the blood equally well. Early killing (0 to 48 h) of S. typhimurium in the liver and spleen is mainly macrophage mediated, and mice infected with trypanosomes kill S. typhimurium in the liver and spleen very poorly. Apparently trypanosomiasis inhibits macrophage bactericidal activity, but has no effect on phagocytosis.

Animals↗
PubMed1984

Quantitative analysis of Fc gamma receptors on murine spleen cell populations by using dual parameter flow cytometry.

The expression of Fc gamma R on subsets of mouse spleen cells was examined by dual parameter flow microfluorometry. B cells were detected by labeling them with antibodies against sIgM, sIgD, sIgG, or I-A; essentially all B cells expressed Fc gamma R. The number of Fc gamma R per cell on the sIgD+, sIgM+, and I-A+ cells averaged 2 X 10(4) receptors, and no correlation between the levels of expression of Fc gamma R and the B cell markers was evident. The sIgG+ B cells, however, expressed more Fc gamma R (8 X 10(4) receptors/cell) than sIgM+ and sIgD+ B cells. Fc gamma R on splenic macrophages were examined by double labeling spleen cells for Fc gamma R and Mac-1. The Mac-1+ cells (2 to 16% of the spleen cells) were 100% Fc gamma R+ and expressed threefold to fivefold higher numbers of Fc gamma R per cell than the sIgM+ or sIgD+ B cells. The Fc gamma R on T cells were studied on cells double labeled for Fc gamma R and Thy-1, Lyt-1, or Lyt-2. An average of 20% of the T cells expressed Fc gamma R and at least two subsets of Fc gamma R+ T cells were evident: Lyt-2- cells, most of which expressed intermediate (2 X 10(4) Fc gamma R/cell) levels of Fc gamma R, and Lyt-2+ cells, which expressed mainly high (8 X 10(4) Fc gamma R/cell) amounts of Fc gamma R. The levels of expression of Fc gamma R and sIgM increased dramatically in response to infection and were elevated in mice with genetic defects. We conclude that the level of Fc gamma R expression is a characteristic property of subsets of spleen cells from normal and infected mice.

Animals↗
PubMed1984

In vivo and in vitro responses to sheep erythrocytes by lymph node cells from mice with trichinellosis.

Mice infected with Trichinella spiralis for 20 days have decreased numbers of plaque forming cells (PFC) in the draining lymph nodes following subcutaneous immunization with sheep erythrocytes. However, when immunized in vitro, lymph node cells from infected mice generate more PFC than normal controls. Splenectomy has no effect on suppression observed in vivo. There is a large increase in the proportion and numbers of B cells in the lymph nodes of infected mice, and these cells may account for the enhanced PFC responses in vitro.

Animals↗
PubMed1983

Serum interferon in Navajo children with severe combined immunodeficiency disease inhibits lymphoblastogenesis.

Two Navajo Indian children with severe combined immunodeficiency disease (SCID) lost reconstituted immune function after virus infections. A serum factor which inhibited normal lymphocyte response to mitogens was found in one of them and led to the examination of sera from five other Navajos with SCID. Mean inhibition by six Navajo sera was 67%; no inhibitor was found in sera from normal adults and children. The inhibitor activity was nondialyzable and heat stable, yet partially sensitive to pH 2.0, suggesting that interferon(s) was present. Interferon (IFN) activity in patient sera ranged from 10 to 300 U/ml. Normal children had peak serum IFN levels of 100 and 30 U/ml in the acute and convalescent periods, respectively, of virus infections. IFN alpha, IFN beta, and IFN gamma were identified in SCID sera by specific antisera. Both inhibitor and IFN activities in three Navajo sera were 88-95 and 89-100%, respectively, removed with anti-IFN antisera. Similar patterns of inhibition of lymphoblastogenesis were seen with IFN standards. IFN levels in the SCID patients did not correlate with documented infections; elevated levels were present when no infections could be documented. The immunologic imbalances in some forms of SCID may be related to circulating inhibitors, possibly interferon.

Arizona↗
PubMed1983

Age-related changes in mitogen-induced lymphocyte function from birth to old age.

This study examines the relationship between age and mitogen-induced lymphocyte blastogenesis. Lymphocytes were stimulated with PHA; Concanavalin A (Con A), and PWM in 156 normal, healthy subjects ranging in age from birth to 75 years. The findings indicate a gradual but significant decrease in PHA- and Con A-induced blastogenesis with increasing age. The decrease in Con A and PHA induced in vitro lymphocyte function begins in early childhood and young adulthood, respectively, and continues throughout the age range studied. In addition, there appears to be a decreased range of lymphocyte functional capacity among the 50-75-year-old subjects. The clinical and laboratory implications of these observations are discussed.

Adolescent↗
PubMed1983

Trypanosomiasis in mice with naturally occurring immunodeficiencies.

By using mice with naturally occurring defects, we have shown that an intact macrophage system is crucial to survival with the pathogenic protozoan Trypanosoma rhodesiense, since a defect in these cells decreased survival by half. Deficiencies in natural killer cell function or complement levels had no effect on survival. However, the capacity to survive trypanosomiasis was not related to the levels of parasitemia achieved during infection.

Animals↗
PubMed1983

Development of the spleen.

Embryogenesis and later development of the spleen's hematologic and immune functions involves ingrowth of vascular channels, influx of reticular cells and related byproducts to form a filtering network, migration of cells from other organs such as bone marrow and thymus, and final maturation of transient and resident cell populations.

Animals↗
PubMed1983

Age-related changes in T- and B-lymphocyte subpopulations in the peripheral blood.

Quantitation of T and B lymphocytes in infants and children is an important test in the diagnosis of a suspected immuno-deficiency. Previous studies indicated that the absolute and relative numbers of lymphocyte subpopulations vary with age, but these data in the pediatric age group are incomplete and often contradictory. We reviewed the literature and investigated the relationship between age and lymphocyte subpopulations in healthy infants and children using common methods and recent methodologic improvements. We found that absolute numbers of T and B cells followed the same trend as the total lymphocyte count, which was elevated at birth, increased in the first six months, and then gradually decreased to adult levels at approximately 13 years of age. Compared with adult values, the percentage of B cells also was higher at birth and continued to increase for six months, followed by a gradual decrease to adult levels by late childhood or early adolescence. The percentage of T cells gradually increased to adult levels by the same age range.

Adolescent↗
PubMed1982

Pollen-induced chemiluminescence: inhibition by serum from allergic individuals.

The interaction between pollen grains, polymorphonuclear leukocytes (PMNs) and serum results in the formation of "pollen rosettes" and the production of chemiluminescence (CL). Significantly more CL is produced by cells exposed ot pollen and sera from nonallergic individuals compared with sera from allergic individuals. The source of the PMNs, however, has no effect on the CL produced, When IgG is isolated from the sera of allergic individuals and added to the test system, a large CL response is seen that is inhibited by the IgG-depleted fraction. No similar inhibition is produced by the IgG-depleted fraction of sera from nonallergic individuals. The inhibitor of CL in sera from allergic individuals appears to be IgE, since its removal leads to an enhanced CL response. These results suggest that competition for a limited number of binding sites on pollen grains exists between pollen specific IgG and IgE antibodies in serum from allergic patients.

Granulocytes↗
PubMed1982

Interactions of Neisseria gonorrhoeae with human neutrophils: effects of serum and gonococcal opacity on phagocyte killing and chemiluminescence.

Serum-sensitive strains of Neisseria gonorrhoeae were incubated with suspensions of normal or chronic granulomatous disease human neutrophils in the absence or presence of fresh or heat-inactivated human serum; phagocytosis, gonococcal viability, and chemiluminescence were measured. Nonpiliated opaque or transparent gonococci (colony types 3 and 4, respectively) were used for phagocytic bactericidal assays. In the presence of 2.0% fresh human serum, normal neutrophils killed >90% of types 3 and 4 gonococci by 135 min. Serum alone at this concentration was not bactericidal. In the absence of serum, type 4 gonococci were not killed, whereas type 3 gonococci were killed to the same degree as in the presence of serum. Interestingly, heat-inactivated normal serum slightly inhibited phagocytic killing of type 3 gonococci. Results almost identical to those above were obtained when 5% fresh human serum deficient in complement component 7 was substituted for 2% normal autologous serum. This indicated that the later components of complement were not involved in the observed results. To investigate the mechanisms responsible for the intracellular killing of the gonococci, we used neutrophils from patients with chronic granulomatous disease. These neutrophils are deficient in an activable NADPH oxidase and do not produce bactericidal oxygen products upon phagocytic stimulation. Neutrophils from two unrelated boys with chronic granulomatous disease killed type 3 and 4 gonococci to the same degree as did normal neutrophils. As with normal neutrophils, serum was needed for killing type 4 organisms. As expected, neutrophils from these patients showed absolutely no increased chemiluminescence in the presence of type 3 or 4 gonococci, with or without serum. The effects of serum on gonococcus-induced chemiluminescence by normal neutrophils was also investigated. For these studies, in addition to type 3 and 4 gonococci, we also used transparent colony types of lightly (type 1) and heavily (type 2) piliated organisms. Chemiluminescence induced by type 1, 2, or 3 gonococci (i.e., gonococci possessing either pili or opacity-associated proteins, but not both) was augmented only slightly by serum and then only at low ratios of gonococci to neutrophils. On the other hand, chemiluminescence induced by type 4 gonococci (i.e., gonococci possessing neither pili nor opacity-associated proteins) was substantially increased in the presence of serum. Stimulation of chemiluminescence by type 1, 2, 3, or 4 gonococci was dose dependent in the absence or presence of serum. Heat-killed type 3 gonococci induced chemiluminescence to the same degree as did viable organisms. Since the gonococci used in this research was strongly catalase positive, as are gonococci in general, and since it was killed by chronic granulomatous disease neutrophils, the results indicate that gonococci can be effectively killed within neutrophils, i.e., within phagolysosomes, by nonoxidative bactericidal mechanisms. Whereas type 3 gonococci were phagocytized and killed by neutrophils equally well with or without serum, serum was obligatory for phagocytic killing of type 4 gonococci, i.e., gonococci lacking opacity-associated proteins. In addition, either pili or opacity-associated proteins were apparently necessary for maximal stimulation of neutrophil chemiluminescence. The submaximal stimulation of chemiluminescence by gonococci lacking both pili and opacity-associated proteins, i.e., type 4 gonococci was augmented by low concentrations of nonimmune serum.

Bacterial Proteins↗
PubMed1982

Interactions between human neutrophils and vaccinia virus: induction of oxidative metabolism and virus inactivation.

The possible role of human neutrophils (PMN) as direct effector cells against free live virus particles was tested in vitro. Oxygen consumption, production of chemiluminescence and "virus killing" by PMNs was examined during and after incubation of cells and live or dead vaccinia virus with and without specific antibody. Oxygen consumption and chemiluminescence production occurred with unopsonized live but not with inactivated virus and was greatly enhanced with opsonization. Virus titers were determined in PMN-free supernatant and freeze-thawed cell pellet fractions after 15 min incubation. Reduction in titer from virus control was seen in supernatant fractions with and without opsonins, but in the cell fraction only with opsonins; the degree of reduction with opsonins was directly related to the opsonin source. PMNs from a patient with chronic granulomatous disease did not inhibit virus replication. These data suggest an active role for human PMNs in the genesis of and defense against virus infections and indicate areas for further investigation.

Antibodies, Viral↗
PubMed1981

In utero Epstein-Barr virus (infectious mononucleosis) infection.

A male infant infected in utero with Epstein-Barr virus (EBV) demonstrated a syndrome of multiple congenital anomalies (micrognathia, cryptorchidism, central cataracts), hypotonia, thrombocytopenia, persistent monocytosis, proteinuria, and multiple areas of metaphysitis at birth. Lymphocytes were Epstein-Barr nuclear antigen (EBNA) positive (18%) and persisted in culture for three months. He had antibody to early antigen (anti-EA), IgM-viral capsid (anti-VCA), and EBNA (anti-EBNA) detectable at 22 days of age. All attempts to isolate infectious agents or to serologically identify other infectious causes for his syndrome were negative.

Abnormalities, Multiple↗
PubMed1981

Treatment of childhood combined Epstein-Barr virus/cytomegalovirus infection with oral bovine transfer factor.

An illness lasting for two years, with recurrent fever, rash, abdominal pain, and arthralgia, developed in a four year old boy. He was found to have a combined Epstein-Barr virus and cytomegalovirus (CMV) infection. His symptoms, CMV in his urine, and an absent in vitro lymphocyte response to CMV antigen persisted for two years. After treatment with orally administered bovine transfer factor clinical symptoms and viruria disappeared and specific immunity to CMV developed. Evaluation of this treatment in chronic virus infections is warranted.

Antibodies, Viral↗