Studies on Inflammation

The origin of the polymorphonuclear leucocytes found in the intermediary and subcapsular sinuses of the popliteal lymph node during acute bacterial lymphadenitis, and the effect of this leucocyte infiltration on the passage of bacteria through the lymph node have been investigated. It has been demonstrated that: 1. The polymorphonuclear leucocytes in the nodal sinuses originate both from blood vessels of the lymph node and from the primary inflammatory focus in the tissues. 2. Granulocytes invading the intermediary sinuses of the infected lymph node arise primarily from capillaries lining these sinuses. 3. Most of the polymorphonuclear leucocytes in the subcapsular sinus, on the other hand, originate from the inflammatory focus in the tissues and appear to traverse the node by way of this peripheral sinus. 4. The bacteremia following direct intralymphatic injection of pneumococci is suppressed by the presence of preformed inflammatory exudate in the nodal sinuses indicating that the filtering capacity of the node is thereby greatly increased.

Section: The Relationship Of the Inflammatory Exudate In The Nodamentioning

confidence: 99%

mentioning

confidence: 99%

Cellular Mechanisms of Antibacterial Defense in Lymph Nodes

Smith¹,

Wood²

1949

“…Although many aspects of the pathological changes occurring in the lymphatic system during acute bacterial infection have been described in detail (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15), the cellular reactions noted in lymph nodes during inflammation, and their relationship to the initial bacterial lesion have never been systematically investigated. The most extensive study of bacterial lymphadenitis is that of Benzan~on and Labb6 (16,17), who noted granulocytic infiltration in the nodal sinuses of animals infected with Bacillus anthracis, Staphylococcus aureus, and Corynebacterium diphtheriae and described diapedesis of leucocytes from capillaries within the regional nodes.…”

mentioning

confidence: 99%

Cellular Mechanisms of Antibacterial Defense in Lymph Nodes

Smith¹,

Wood²

1949

Acute pneumococcic lymphadenitis produced in rats by intradermal inoculation of the foot-pad is characterized by rapid infiltration of polymorphonuclear leucocytes into the intermediary sinuses of the node, and prompt phagocytosis of pneumococci by both the macrophages of the sinuses and the recently arrived leucocytes. After 5 to 7 hours the polymorphonuclear leucocytes are found densely congregated about the hilar region, and 9 hours after inoculation most of the phagocyted organisms have been digested. At the end of the 24 hour period the popliteal node presents the picture of a subsiding inflammation with a marked macrophage reaction and regenerating lymph follicles. Phagocytosis of encapsulated pneumococci in the foot-pad and popliteal node occurs in less than 30 minutes after inoculation. It is assumed that this prompt phagocytosis is effected by the non-antibody mechanism of "surface phagocytosis." The majority of polymorphonuclear leucocytes that enter the sinuses of the inflamed node appear to come from capillaries within the node itself rather than from the primary site of inflammation in the foot-pad. The prompt inflammatory response of the nodal tissues serves as an active defense against lymph-borne infection. Macrophages invade nodal sinuses only after most of the pneumococci have been destroyed by polymorphonuclear leucocytes. It is suggested that the macrophage reaction follows removal of the primary inflammatory stimulus by the granulocytes, and thus constitutes only a late phase of recovery. Fibrin formation in the sinuses of the lymph node is rare during acute lymphadenitis. This finding may be related to the observation that within 5 minutes after entrance of bacteria into the node, heparin-containing granules from mast cells are strewn throughout the sinuses.

“…Opie (1) and Menkin (2)(3)(4)(5)(6) have demonstrated that various materials are fixed in situ when injected into an acutely inflamed area, and Menkin has emphasized the r61e of mechanical obstruction in the form of a fibrinous network and thrombosed lymphatics in the fixation of such substances as bacteria and trypan blue as an important factor in the resistance of tissues to invasion. Recently, Menkirl (6) has ascribed the characteristic lack of invasiveness of Staphylococcus aureus to the irritating properties of that organism which induce a prompt inflammatory response as shown by the early fixation of trypan blue.…”

mentioning

confidence: 99%

A Study on the Mechanism of Invasiveness of Streptococci

Dennis

Berberian

1934

Opie (1) and have demonstrated that various materials are fixed in situ when injected into an acutely inflamed area, and Menkin has emphasized the r61e of mechanical obstruction in the form of a fibrinous network and thrombosed lymphatics in the fixation of such substances as bacteria and trypan blue as an important factor in the resistance of tissues to invasion. Recently, Menkirl (6) has ascribed the characteristic lack of invasiveness of Staphylococcus aureus to the irritating properties of that organism which induce a prompt inflammatory response as shown by the early fixation of trypan blue. On the other hand, the fixation of trypan blue in inflamed areas produced by Streptococcus haemolyticus was delayed about 45 hours, which led him to suggest that the greater invasiveness of this organism may be due to its lack of irritating properties and consequent delay in inflammatory response, thus leaving the lymphatics open as available routes for dissemination.The experimental data set forth below indicate that the supposed paradox is illusory. Menkin's observations (6) are fully confirmed as to the behavior of staphylococcus and streptococcus in the skin of rabbits, but the delay of inflammatory fixation of trypan blue by streptococci probably is due to the production of two substances, one of which is fibrinolyfic, while the other acts by inhibiting fibrin formation. Experimental evidence is given for the existence of these two substances, and certain of their properties are described. The effects of cultures and filtrates of certain distinct strains of Streptococcus haemolyticus, Streptococcus viridans, and Staphylococcus aureus on the fixation