Kenneth Wertman

Complement-fixing murine typhus antibodies in vitamin deficiency states.

Summary These studies indicate that rats on a diet containing what is considered to be an optimum vit. B complex content have the ability to produce circulating complement fixing antibodies when immunized with relatively large amounts of the rickettsiae of murine typhus fever. Likewise, rats maintained on a diet containing only one-tenth of the presumed optimum also have the ability to produce these same antibodies to approximately the same titers. Pantothenic acid and thiamin deficiencies influenced the antibody response when a relatively small amount of immunizing material was injected. The influence is not as apparent when relatively large amounts of the antigenic material was employed.

Complement-fixing murine typhus antibodies in vitamin deficiency states. III. Riboflavin and folic acid deficiencies.

Summary 1. It appears as though the riboflavin requirement for antibody production is not as critical as the folic acid requirement. 2. This study indicates that both riboflavin and folic acid deficiencies impaired the production of circulating complement-fixing antibodies when relatively small amounts of antigen were injected. However, after more antigen was introduced, significant titers were obtained from the sera of riboflavin deficient rats but the folic acid deficient animals produced significantly less antibody. The inanition control (paired-weighed) and the normal control animals (fed ad libitum) demonstrated antibody production of approximately the same titers when injected with either 0.0073 mg N or 0.0365 mg N. Therefore, it appears as though the specific vitamin deficiency and not the inanition is the significant factor in the production of circulating complement-fixing antibody.

Complement-Fixing Murine Typhus Antibodies in Vitamin Deficiency States. II. Pyridoxine, and Nicotinic Acid Deficiencies

Summary These studies indicate that nicotinic acid deficiency does not appreciably influence the production of circulating complement-fixing antibody when either relatively small or large amounts of antigenic stimulation were employed. Pyridoxine deficiency, however, influenced unfavorably the antibody response when either small or large amounts of the antigen were injected. The single immunizing injection (0.0073 mg N) did not bring forth circulating antibodies that were demonstrable by complement-fixation.

Complement-Fixing Murine Typhus Antibodies in Vitamin Deficiency States. IV. B12 Deficiency.

Summary This study indicates that a vit. B12 deficiency impaired the production of circulating complement-fixing antibody. The sera of the inanition control and the ad libitum control animals possessed antibody concentrations of approximately the same titers. This was evident when either 0.0073 mg N or 0.0365 mg N was employed as the antigen. Therefore, the specific vitamin deficiency and not inanition appears to be the significant factor affecting the production of circulating complement-fixing antibody under these experimental conditions.

The Effects of Vitamin Deficiency on Some Physiological Factors of Importance in Resistance to InfectionIII. Vitamin B12 and Folic Acid Deficiencies

Male white rats were maintained on a well defined diet deficient in niacin and tryptophane, and various physiological factors of resistance to infection were studied. Adequate inanition and ad libitum control animals were included in the investigation. The following physiological factors were studied: (1) cellular composition of the peripheral blood, (2) complement activity, (3) cellular migration in inflammation, (4) cellular composition of the exudate in inflammation, (5) leukotaxine activity, and (6) cellular composition of bone marrow. The following observations were made from these studies: 1. (1) no significant difference was noted in the total number of erythrocytes and leukocytes per mm3 of blood in the vitamin deficient, inanition and ad libitum control groups. 2. (2) the differential cell counts of the blood film preparations suggested a percentage increase in polymorphonuclear leukocytes in both the niacin-tryptophane deficient animals and the inanition control rats. In the blood specimens of most of these animals, a slight reduction in the percentage of lymphocytes was evident. 3. (3) complement activity could not be demonstrated in the sera of the niacin-tryptophane deficient rats even though amounts sixteen times greater than those of the ad libitum controls were employed. 4. (4) cellular migration to an inflamed area was considerably reduced in the niacin-tryptophane deficient and inanition control animals as compared with ad libitum controls. 5. (5) a relative granulocytosis and lymphopenia were observed in the exudates removed from the inflamed areas of the inanition and niacintryptophane deficient animals as compared with the exudates from the ad libitum control rats. 6. (6) no alteration in capillary permeability, as measured by the Menkin dye accumulation technique, was noted even though significant differences in cellular migration occurred. 7. (7) the bone marrow preparation made from the tibia of the inanition control rats presented a lymphopenia as compared with the ad libitum control smears. The bone marrow of the niacintryptophane deficient rats presented a similar picture.